\r\n\t• Role of technological innovation and corporate risk management \r\n\t• Challenges for corporate governance while launching corporate environmental management among emerging economies \r\n\t• Demonstrating the relationship between environmental risk management and sustainable management \r\n\t• Contemplating strategic corporate environmental responsibility under the influence of cultural barriers \r\n\t• Risk management in different countries – the international management dimension \r\n\t• Global Standardization vs local adaptation of corporate environmental risk management in multinational corporations. \r\n\t• Is there a transnational approach to environmental risk management? \r\n\t• Approaches towards Risk management strategies in the short-term and long-term.
",isbn:"978-1-83968-906-2",printIsbn:"978-1-83968-905-5",pdfIsbn:"978-1-83968-907-9",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"9b65afaff43ec930bc6ee52c4aa1f78f",bookSignature:"Dr. Muddassar Sarfraz and Prof. Larisa Ivascu",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10226.jpg",keywords:"Global Risk Management, Risk Assessment, Climate Risk, Environmental Management, International Business, Business Sustainability, Corporate Governance, Financial Market, Financial Risks, Sustainable Economic Environment, Business Valuation, Organizational Behavior",numberOfDownloads:131,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"September 24th 2020",dateEndSecondStepPublish:"October 22nd 2020",dateEndThirdStepPublish:"December 21st 2020",dateEndFourthStepPublish:"March 11th 2021",dateEndFifthStepPublish:"May 10th 2021",remainingDaysToSecondStep:"4 months",secondStepPassed:!0,currentStepOfPublishingProcess:4,editedByType:null,kuFlag:!1,biosketch:"Dr. Muddassar Sarfraz focuses on corporate social responsibility, human resource management, strategic management, and business management. He is a member of the British Academy of Management (UK), Chinese Economists Society (USA), World Economic Association (UK), American Economic Association (USA), and an Ambassador of the International MBA program of Chongqing University, PR China, for Pakistan.",coeditorOneBiosketch:"Dr. Larisa Ivascu's area of research includes sustainability, management, and strategic management. She has published over 190 papers in international journals. She is vice-president of the Society for Ergonomics and Work Environment Management, Timisoara, and a member of the World Economics Association (WEA), International Economics Development and Research Center (IEDRC), Engineering, and Management Research Center (CCIM).",coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"260655",title:"Dr.",name:"Muddassar",middleName:null,surname:"Sarfraz",slug:"muddassar-sarfraz",fullName:"Muddassar Sarfraz",profilePictureURL:"https://mts.intechopen.com/storage/users/260655/images/system/260655.jpeg",biography:"Dr Muddassar Sarfraz is working at the Binjiang College, Nanjing University of Information Science and Technology, Wuxi, Jiangsu, China. He has obtained his PhD in Management Sciences and Engineering from the Business School of Hohai University. He holds an International Master of Business Administration (IMBA) from Chongqing University (China) and Master of Business Administration (HR) from The University of Lahore. He has published tens of papers in foreign authoritative journals and academic conferences both at home and abroad.\nHe is the Book Editor of Sustainable Management Practices, Analyzing the Relationship between Corporate Governance, CSR, Sustainability, and Cogitating the Interconnection between Corporate Social Responsibility and Sustainability. He is the Associate and Guest Editor of Frontiers in Psychology, International Journal of Humanities and Social Development Research and the Journal of Science and Innovative Technologies. He is an Editorial Board Member of the International Journal of Human Resource as well as a member of the British Academy of Management (UK), Chinese Economists Society (USA), World Economic Association (UK), American Economic Association (USA), and an Ambassador of the International MBA program of Chongqing University, PR China, for Pakistan. \nHis research focuses on corporate social responsibility, human resource management, strategic management, and business management.",institutionString:"Binjiang College, Nanjing University of Information Science &Technology, Wuxi, Jiangsu",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"1",institution:null}],coeditorOne:{id:"288698",title:"Prof.",name:"Larisa",middleName:null,surname:"Ivascu",slug:"larisa-ivascu",fullName:"Larisa Ivascu",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRfMOQA0/Profile_Picture_1594716735521",biography:"Dr Larisa IVAȘCU is currently an associate professor at the Politehnica University of Timisoara. 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From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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\n
1. Introduction
\n
\n
1.1. The fruit fly, Drosophila melanogaster, as a model for innate immunity
\n
Immunity is a vital component in understanding host‐pathogen relationships. It is composed of two responses: innate and adaptive. Innate immunity recognizes morphological characteristics of pathogens for immediate antimicrobial and antiviral defense [1]. Adaptive immunity develops during infection to produce immunological memory against pathogens. This memory provides an immediate pathogen‐specific defense against future infections of the same pathogen [2]. Most vertebrate organisms utilize both immune responses for pathogen defense. However, the fruit fly, Drosophila melanogaster, does not have an adaptive immune response and relies solely on an innate immune response [3]. This provides a powerful model system to better understand the interaction between innate immunity and pathogenic infections.
\n
Innate immunity is composed of various pathways that target bacteria, fungi, and viruses. These pathways include the immune deficiency pathway (Imd), Toll‐Dorsal pathway (Toll), Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT), autophagy, and RNA interference (RNAi) [3, 4, 5, 6]. The Imd and Toll pathways contribute to the antibacterial and antifungal defense. However, their function in antiviral defense is not fully understood [7, 8]. The JAK/STAT, autophagy, and RNAi pathways contribute to antiviral defense, with RNAi as the main contributor for antiviral defense.
\n
\n
\n
1.2. Drosophila viruses
\n
As a model organism, D. melanogaster is used to study host immunity to pathogen interactions. Most research is focused on the interaction between bacteria, fungi, and the D. melanogaster innate immune response, but viruses are a subject of current interest. Populations of Drosophila have naturally occurring infections of RNA viruses, such as Nora virus, Sigma virus (DmelSV), Drosophila C virus (DCV), and Drosophila X virus (DXV). In addition, the first naturally occurring DNA virus, Kallithea virus, is found in D. melanogaster (\nTable 1\n) [9, 10, 11, 12, 13].
\n
\n
\n
\n
\n
\n
\n\n
\n
Virus
\n
Family
\n
Genome nucleic acid
\n
Mode of transmission in D. melanogaster\n
\n
Effects of infection
\n
\n\n\n
\n
Nora virus
\n
\nPicornavirales\n
\n
(+) ssRNA
\n
Horizontal
\n
No documented pathology, slight effect on longevity [14]
Nora virus is a recently discovered picorna‐like D. melanogaster virus. The virus is sequenced and has a 12 kilobase (kb), single‐stranded, positive‐sense RNA genome. Viral particles measure 30 nm in diameter and are non‐enveloped [9]. It establishes a persistent infection in natural and laboratory populations of D. melanogaster with no known effect of viral load and no display of pathology on the fly. The virus is transmitted horizontally through the fecal‐oral route with infection localizing to the intestinal tract [14]. The genome is organized into four open reading frames (ORFs), unlike other picorna‐like viruses such as DCV, which has two ORFs [15]. ORF1–3 partially overlaps, suggesting ribosomal frame shifting events during translation. However, an 88 nucleotide region is found between ORF3 and ORF4, suggesting that an independent initiation translation event is occurring [16]. ORF1 encodes a highly charged protein, which is a suppressor of RNAi [17]. ORF2 encodes a picorna‐like replicative cassette, which consists of a helicase, protease, and RNA‐dependent RNA polymerase [9]. The hypothesized major capsid proteins of Nora virus are products of ORF3 and ORF4 at the 3′ end of the genome. ORF3 encodes VP3, which is crucial for the stability of Nora virus virions [18]. ORF3 is not fully characterized, but certain aspects of its protein products were predicted using bioinformatics. It has a predicted alpha‐helical domain as a key structural motif [9]. ORF4 is processed into three major proteins, VP4A, VP4B, and VP4C. VP4A and VP4B are predicted to form jelly roll folds, which are also found in other capsid proteins of Picornavirales. The third protein, VP4C, has a predicted alpha‐helical structure and is also a structural component of the virus [16].
\n
Another virus naturally occur in D. melanogaster is Sigma virus. Sigma virus belongs to the family Rhabdoviridae [10]. It is composed of a negative‐sense, single‐stranded RNA genome that consists of five genes: N, P, M, G, and L. The gene N is a nucleoprotein, P is the polymerase‐associated protein, M is the matrix protein, G is the glycoprotein, and L is the polymerase [19]. A sixth gene, X, exists between P and M, but its current function is not fully understood [20]. In natural infections, the virus causes paralysis or death if flies are exposed to CO2. It is passed through vertical transmission through the sperm or eggs and is the only known host‐specific pathogen of D. melanogaster [10, 20].
\n
Drosophila C virus is in the family Dicistroviridae [21]. The virus particle measures 30 nm in dm with a 9264 kb, positive‐sense, single‐stranded RNA genome [22]. The genome consists of two ORFs separated by 191 nucleotides. ORF1 encodes an RNA‐dependent RNA polymerase, helicase domain, and protease domain [15]. Also, an RNAi suppressor, DCV‐1A, is encoded at the N‐terminus of ORF1. The suppressor binds long dsRNA, which inhibits Dicer‐2 (Dcr‐2) processing [23]. ORF2 encodes the structural proteins VP0, VP1, VP2, VP3, and VP4. VP0 is a precursor for VP3 and VP4, which combine to form the capsid [24]. The capsid proteins are encoded in a different reading frame and initiated independently from ORF1 [15]. In addition, DCV is a naturally occurring pathogen found within D. melanogaster and spread through horizontal transmission by infected flies or contaminated food. Viral infection can be lethal if injected, but naturally infected flies display decreased pathogenicity [11].
\n
\n\nDrosophila X virus is a double‐stranded RNA virus, which belongs to the family Birnaviridae. It was discovered in a study involving D. melanogaster and Sigma virus. Like Sigma virus, DXV is pathogenic, induces CO2 sensitivity, and is lethal [12]. The virus displays a non‐enveloped capsid and a bi‐segmented dsRNA genome. Segment A encodes a polyprotein, which forms the capsid. The capsid consists of VP1, preVP2, VP2, VP3, and VP4. Segment B encodes VP1, an RNA‐dependent RNA polymerase [25].
\n
Recently, a DNA virus was discovered in wild populations of Drosophila. By using a metagenomic approach, the Kallithea virus was identified. The virus is closely related to D. innubila and the beetle Orcytes rhinoceros Nudiviruses. In addition, this is the first DNA virus found naturally occurring in D. melanogaster. However, the virus has not been characterized in D. melanogaster with recent research using other Drosophila species [13]. In wild D. innubila, Nudivirus infection is associated with greatly reduced survival and offspring production. In wild D. falleni, infection resulted in greatly reduced offspring production. Additionally, infection is highly pathogenic and mediated through the fecal‐oral route [26]. Further research with naturally occurring Drosophila viruses is important because not many of these viruses exist or have been discovered.
\n
\n
\n
1.3. Non‐Drosophila viruses
\n
Laboratory populations of D. melanogaster can be experimentally inoculated with RNA viruses, such as Cricket paralysis virus (CrPV), Flock House virus (FHV), Sindbis virus (SINV), and Vesicular stomatitis virus (VSV). Also, the DNA virus, Invertebrate iridescent virus 6 (IIV‐6), can be experimentally inoculated into flies (\nTable 1\n) [27, 28, 29, 30, 31]. Artificial infections of D. melanogaster allow for a better understanding and novel insights of host‐pathogen interactions.
\n
Cricket paralysis virus is a positive‐sense, single‐stranded RNA virus closely related to DCV. It belongs to the family Dicistroviridae and was first discovered in field crickets, Teleogryllus oceanicus and T. commodus [32]. The crickets displayed rapid paralysis and significant mortality [27]. The viral RNA genome consists of two ORFs, ORF1 and 2. To initiate translation, each ORF requires an internal ribosome entry site (IRES) region. ORF1 encodes non‐structural replication proteins, and ORF2 encodes structural proteins, which form the viral capsid. In addition, this virus encodes a suppressor of RNAi, CrPV‐1A, which binds to Argonaute‐2 (AGO2) inhibiting RNA‐induced silencing complex (RISC) activity [32].
\n
Flock house virus contains two positive‐sense, single‐stranded RNAs within a non‐enveloped virion. This virus belongs to the Nodaviridae family and was first discovered in the grass grub, Costelytra zealandica [28, 33]. Viral inoculation kills D. melanogaster, and the virus propagates in D. melanogaster cell lines [34]. The bipartite genome consists of RNA1 and RNA2. RNA1 encodes protein A, an RNA‐dependent RNA polymerase, whereas RNA2 encodes the precursor protein for production of the mature capsid protein. For viral replication, both RNAs must be present within the cell or replication will not occur [35]. A subgenomic RNA, RNA3, is produced by RNA1 and encodes an RNAi suppressor protein B2. The protein binds viral dsRNA to protect it from cleavage by Dcr‐2 and to inhibit loading of viral siRNAs into the RISC complex [34, 36, 37].
\n
Sindbis virus is a single‐stranded, positive‐sense RNA virus, belongs to the Togaviridae family, and is transmitted vertically in Drosophila. In other hosts, it is transmitted horizontally. The viral genome mimics cellular mRNA as the viral mRNA possesses a 5′ methylguanylate cap and a 3′ poly(A) tail. The 5′ region encodes nonstructural proteins, and the 3′ region encodes viral structural proteins [38]. Most Sindbis virus research with invertebrates is conducted with mosquitoes because they are a natural vector for SINV. However, D. melanogaster S2 (Schneider 2) cells are successfully infected establishing an additional invertebrate model system to examine the host‐pathogen interaction with SINV [29].
\n
Vesicular stomatitis virus is a single‐stranded, negative‐sense RNA virus that belongs to the Rhabdoviridae family [30]. It belongs to the same family as Sigma virus, which naturally occurs in Drosophila [39]. The genome is composed of the structural proteins (G, N, and M), the minor protein (NS), the partially glycosylated G precursor (G1), and the L chain. Insects infected with VSV become paralyzed after exposure to CO2. However, VSV has no observable pathogenic effects in infected insect cells [30, 40].
\n
Invertebrate iridescent virus 6, also known as Chilo iridescent virus, is a large and complex double‐stranded DNA virus that belongs to the Iridoviridae family. The virus is composed of a capsid, an intermediate lipid layer, and a viral genome composed of linear double‐stranded DNA [41]. The viral genome size is approximately 212.5 kb, circular, and encodes 211 ORFs along both strands [31]. Several important ORFs encode a DNA‐dependent RNA polymerase II, a helicase, and major capsid proteins [42]. IIV‐6 has a broad host range and can be used to experimentally infect D. melanogaster. Infections in D. melanogaster produce high and stable viral titers exhibiting a low mortality rate [31]. Artificial infections of D. melanogaster are important because they provide a valuable model of understanding interactions between virus and host immunity.
\n
\n
\n
\n
2. RNA interference (RNAi) and the immune response
\n
\n
2.1. Antiviral RNAi in D. melanogaster\n
\n
RNAi is the major antiviral immune response pathway for D. melanogaster (\nFigure 1\n). The general pathway occurs in two steps, initiation and execution. To initiate RNAi, dsRNA must be introduced, such as with viral infection. If dsRNAs are greater than 23 bp in length, it is processed into 21–23 bp dsRNA fragments with 3′ overhanging ends by Dcr‐1 or Dcr‐2 [5]. Dcr‐2 produces small interfering RNAs (siRNAs), and Dcr‐1 recognizes precursors of micro RNAs (miRNAs). The siRNA products are recruited by AGO2 into the RISC. Once loaded, one of the siRNA strands is degraded in an AGO2‐dependent process involving an endoribonuclease, component 3 promoter of RISC (C3PO) [43]. The single strand in the RISC complex is called the guide strand. It acts as a targeting mechanism for locating complementary mRNA. Matching of the guide strand to the targeted mRNA results in either degradation or inhibition of translation. Degradation occurs if the guide strand completely matches the target mRNA. However, inhibition of translation occurs if there is a small mismatching of base pairs (2–3 bp) [5]. Additionally, RNAi is incorporated in two alternative pathways: the miRNA or piwi RNA (piRNA) pathways. In the miRNA pathway, miRNA and Argonaute‐1 (AGO1) regulate cellular gene expression through different mechanisms, such as cleavage or translational inhibition [44]. The piRNA pathway is involved as a transposon regulatory control mechanism in D. melanogaster testes [45]. However, the siRNA pathway is the major contributor to the RNAi antiviral defense pathway in D. melanogaster.
\n
Figure 1.
The major virus defense pathways of the fruit fly, Drosophila melanogaster. (A) RNA interference (RNAi) is the primary defense mechanism against viruses in invertebrate species. Virus replication results in the production of dsRNA replication intermediates that activate the pathway. R2D2 has two binding sites for dsRNA and in conjunction with the RNaseIII‐like enzyme, Dicer‐2 (Dcr2), will cleave large dsRNAs into small interfering RNAs (siRNA). The Dcr2/R2D2 siRNA complex subsequently interacts with Argonaut‐2 protein, a key component of the RNA‐induced silencing complex (RISC), and transfers the siRNA component to it. The siRNA acts by targeting viral RNA via base pairing, allowing the targeted viral RNA to be degraded by the nuclease action of RISC. (B) The Toll pathway is activated primarily by pathogen‐associated molecular patterns (PAMPs) associated with fungi and Gram‐positive cell wall components. The PAMPs are recognized by cytoplasmic receptors, such as Gram‐negative bacteria binding proteins (GNBP‐1/‐3) and peptidoglycan recognition proteins (PGRP‐SA, ‐SD). These receptors are referred to collectively as pattern recognition receptors (PRRs). Once the PRRs are engaged by their specific PAMPs, they now activate proteases that cleave full‐length Spatzle to an active form that now can be bound by the Toll receptor. With virus activation of this pathway, it is unclear whether virions can directly interact with Toll or must also activate Spatzle. The binding of the Spatzle ligand to the Toll receptor results in signal transduction through the cytoplasmic adaptor protein, MyD88. This ultimately leads to the proteolytic degradation of Cactus, the inhibitor of the NF‐κB‐like transcription factors Dorsal and Dif. With the degradation of Cactus, the Dorsal‐Dif heterodimer is now able to be transported to the nucleus where it acts to activate the transcription of Toll‐regulated genes. (C) The Imd pathway is activated by PAMPs from Gram‐negative bacteria and potentially directly by virions. A transmembrane peptidoglycan receptor protein (PGRP‐LC) binds the PAMPs and transduces a signal to the cytoplasmic adaptor proteins Imd and FADD, which results in the activation of the caspase‐8 like protease, Dredd. Dredd cleaves the NF‐κB‐like transcription factor, Relish, which removes an IκB‐like C‐terminal domain that masks a nuclear localization signal. In addition, Dredd also cleaves Imd, which now allows it to become ubiquitinated. This attracts the Tab2/Tak1 complex that activates the IKK1/IKK2 proteins via phosphorylation. These activated kinases now phosphorylate Relish at multiple sites, especially S528 and S529, which are essential to RNA polymerase II recruitment to Imd‐regulated genes. (D) The JAK/STAT pathway is activated by the interaction of the ligand unpaired (Upd) with the receptor Dome. In the Drosophila immune response, it appears that Upd3, secreted by activated hemocytes, is the preferred ligand for Dome. Most likely, virions are detected by these cells, which in turn secrete Upd3, although direct interaction of virions with Dome has not been ruled out. Once Dome has engaged Upd, it activates, via signal transduction, the Janus kinase Hop, which now is capable of phosphorylating the STAT transcription factors. Phosphorylation of the STAT proteins results in their dimerization and subsequent translocation to the nucleus where they activate the transcription of JAK/STAT regulated genes. (E) Autophagy can also act as a viral defense pathway. In the absence of a ligand for Toll‐like receptor 7 (Toll7), the signal transduction pathway involving phosphatidylinositol‐3 kinase (PI3K), Akt kinase, and Tor (target of rapamycin) kinase is active and autophagy is inhibited. However, if the Toll-7 receptor is engaged by its ligand, in this case a virion component, this results in the inhibition of PI3K, which ultimately results in the inhibition of Tor, which now relieves inhibition of the autophagy pathway, resulting in the destruction of the cell.
\n
\n
\n
2.2. Viral suppression of RNAi
\n
RNAi is an effective antiviral mechanism, but viruses have developed strategies to counteract it using virus‐encoded suppressors of RNAi (VSRs). RNAi suppression depends on the mechanism the VSR uses to target RNAi components and can vary with each virus [16]. For example, Nora virus VP1, the protein product of ORF1, can suppress RNAi. It inhibits slicer activity of mature RISC by hindering targeted catalytic cleavage by AGO2 [46]. In FHV, RNA1 produces a subgenomic RNA3, which encodes B2, an RNAi suppressor protein. B2 has dual functions for suppression. It binds to long dsRNA to inhibit siRNA production and to siRNA to prevent siRNA assembly into RISC [47]. In CrPV, the N‐terminal region of ORF1 encodes the RNAi suppressor protein, CrPV‐1A. It directly interacts with AGO2, which suppresses the catalytic activity of the RISC complex [32]. In the DNA virus IIV‐6, ORF340R encodes a dsRNA‐binding domain (dsRBD), which binds dsRNA. For evasion and suppression, the dsRBD binds to long dsRNA shielding it from Dcr‐2 processing and inhibiting siRNA loading into the RISC complex, respectively [48]. Viral suppression of RNAi creates an ongoing arms race between viruses and the RNAi pathway. As the RNAi pathway adapts to evade viral infections, viruses counter adapt to evade viral antagonists, which leads to further adaptions of the RNAi pathway [16]. However, RNAi does not clear all viral infections in D. melanogaster suggesting that other alternative antiviral mechanisms must exist.
\n
\n
\n
2.3. Vago acts as an RNAi‐independent antiviral mechanism
\n
During viral infection of D. melanogaster, genes are triggered and expressed. One gene of interest is Vago, a 160‐amino acid protein, with a signal peptide and eight cysteine residues. The signal peptide contains a single von Willebrand factor type C (VWC) motif. Proteins containing a single VWC domain typically respond to environmental changes and nutritional status, such as viral infection [49]. In D. melanogaster, Vago functions in response to viral infection [50]. During DCV infection, Vago proteins are important in controlling viral load in the fat body of D. melanogaster, which suggests that it may have a tissue‐specific role. Also, Vago may act as either an antiviral molecule targeting virions or as a cytokine affecting neighboring cells by triggering an antiviral state [51]. Another gene of interest is virus‐induced RNA 1 (vir‐1). This gene is a marker of viral regulation that is regulated by the JAK/STAT pathway [52]. A potential mechanism is suggested including both genes. Viral infection triggers the induction of a cytokine, Vago, which activates the JAK/STAT pathway (\nFigure 2\n). Once activated, virus‐related gene expression is induced, which includes vir‐1 [51].
\n
Figure 2.
Innate immune signaling among several pathways is integrated. The Imd, JAK/STAT, and RNAi virus defense pathways exhibit coordinate expression of anti‐viral genes in Culex mosquitoes. The RNAi pathway (see \nFigure 1\n) through the sensing of dsRNA by Dicer‐2 activates tumor necrosis factor (TNF) receptor‐associated factor (TRAF). TRAF now interacts with the Imd pathway via driving proteolytic cleavage of the N‐terminal region of Relish, allowing the C‐terminal region of Relish to be transported into the nucleus where it acts as a transcription factor on IMD‐regulated genes. One of these genes is Vago, which specifies a small secretory cytokine‐like molecule. Vago is able to engage the JAK/STAT pathway via the Dome receptor (see \nFigure 1\n), leading to the expression of JAK/STAT regulated genes.
\n
Currently, the pathway for activation of Vago begins with induction of RNAi. First, viral infection is detected by Dcr‐2. Dcr‐2 is a viral sensor, which activates the RNAi pathway and Vago expression for antiviral defense (\nFigure 2\n). For Vago, viral RNA interacts with the DExD/H‐box helicase domain on Dcr‐2 activating an inducible antiviral response. This domain is located at the carboxy‐terminal end of the gene and acts as a cytoplasmic sensor of viral RNA [51]. The DExD/H‐box helicase domain also belongs to the same family as the retinoic acid‐inducible gene 1‐like (RIG‐I) receptors in mammals, which function as pattern recognition receptors for intracellular dsRNA during viral infection [53]. In addition, other innate immunity pathways are analyzed to determine their role in the induction of Vago. However, Toll, Imd, and JAK/STAT were unable to induce Vago expression [51]. Currently, the mode of antiviral action of the protein Vago and its role in the RNAi pathway are not fully understood.
\n
Recently, Vago was further investigated in the mosquito, Culex quinquefasciatus. The orthologue gene, CxVago, contributes to antiviral defense during West Nile virus (WNV) infection. In C. quinquefasciatus, Dcr‐2 is also required for induction and up‐regulation of CxVago. The study suggests that CxVago is a stable, secreted cytokine that stimulates an antiviral response in insects by activating the JAK/STAT pathway (\nFigure 2\n). In addition, CxVago induces expression of the Culex orthologue of the D. melanogaster gene vir‐1 during viral infection [49]. Another study was not able to establish a relationship between DCV‐stimulated Vago and induction of vir‐1 in D. melanogaster [51]. However, Vago may induce vir‐1 during viral infection, but in its absence, other unidentified cytokines may also induce vir‐1 expression [49].
\n
A mechanism for the activation of CxVago was proposed (\nFigure 2\n). First, Dcr‐2 senses a viral infection and activates tumor necrosis factor receptor‐associated factor (TRAF). This process activates Relish 2 (Rel2) by dephosphorylation, which allows translocation of the molecule from the cytoplasm into the nucleus. Rel2 is a nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) transcription factor and induces gene expression of CxVago [54]. However, DmVago is not induced in D. melanogaster by members of the NF‐κB family. This may indicate that regulation of DmVago occurs through a similar or alternative mechanism [51]. The induction of Vago is similar to the RIG‐I/TRAF‐6/NF‐κB‐mediated interferon pathway, which is triggered by a viral infection in mammals [54]. Further analysis of the proposed CxVago pathway in D. melanogaster is required to discover the mechanism for antiviral defense. Vago and its associated pathway might be a simplistic interferon response pathway but requires an in‐depth investigation to determine its role in antiviral defense.
\n
\n
\n
\n
3. Autophagy
\n
Autophagy was first characterized in yeast following starvation, as a process by which cells can degrade long‐lived proteins, organelles, and bulk cytoplasm for recycling [55]. Induction of autophagy is both developmentally and nutritionally regulated. When nutrients are sufficient, class I phosphatidylinositol‐3‐kinases (PI3Ks) and the target of rapamycin (TOR) complex act as inhibitors of autophagy. However, under starvation conditions, class III PI3Ks act to stimulate the production of autophagy‐related proteins and induce the autophagy pathway [55] (\nFigure 1\n).
\n
Following induction, a double‐membrane vesicle, the autophagosome, is formed that can sequester cytoplasmic components. Sequestering of the cytoplasmic components is highly regulated by GTPases, phosphatidylinositol kinases, and other various phosphatases. The autophagosome then fuses with the lysosome for the breakdown of the membrane and its contents [56]. In addition, induction of autophagy can occur as an antiviral response during viral infection.
\n
\n
3.1. Antiviral autophagy
\n
Autophagy also plays a direct antiviral role against vesicular stomatitis virus (VSV). D. melanogaster has homologs of 11 yeast autophagy‐related genes and is confirmed for autophagy during development or starvation [57]. D. melanogaster encodes nine Toll receptors. Eight of the Toll receptors are not fully understood but may have roles in innate immunity. Activation of the autophagy pathway requires the interaction of Toll receptor 7, which detects VSV G protein. Once G protein is detected, two toll‐7 receptors dimerize transmitting a signal through their toll‐interleukin‐1 receptor (TFR‐1) domain [6]. The signal transduction is regulated by the Tor kinase, which leads to the induction of autophagy [56]. Autophagy can be induced under starvation conditions or high stress (i.e., viral infection) conditions. This becomes apparent when D. melanogaster S2 cells are infected with VSV and monitored using fluorescent microscopy for autophagy. Cells with mutant autophagy genes have a significantly higher viral titer than those that contain wild‐type autophagy genes [57]. This indicates that autophagy not only plays a critical role in recycling of organelles and proteins during times of starvation, but it may also have an antiviral role as well.
\n
\n
\n
\n
4. Other antiviral response pathways
\n
The Toll pathway controls the dorsal‐ventral patterning within the D. melanogaster embryo and is activated during fungal and Gram‐positive bacterial infections (\nFigure 1\n). During fungal and bacterial infection, pathogen recognition proteins (PRRs) recognize common molecules from each pathogen called pathogen‐associated molecular patterns (PAMPs). Fungi are detected by their glucans by PRR glucan‐binding protein 3 (GNBP3). Gram‐positive bacteria are detected by their cell wall components that contain lysine‐containing peptidoglycan. Recognition requires a combination of different proteins, including peptidoglycan recognition proteins (PGRP)‐SA, PRGP‐SD, and GNBP1 [58]. After recognition, the protein creates a complex, which activates the Toll pathway. PGRP‐SD is not involved in the complex but is required for detection of certain strains of Gram‐positive bacteria. Activation of Toll initiates a protease cascade activating Spätzle (Spz) [59, 60]. Spz is a protein ligand of the Toll receptor. Once activated, Spz induces conformational changes within the receptor to facilitate the recruitment of Drosophila Myd88, Tube, and Pelle, a protein kinase. This leads to the phosphorylation and degradation of Cactus and NF‐κB‐like transcription factors, which allows Dif (Dorsal‐related immunity factor) to translocate to the nucleus. Dif mediates Toll‐dependent gene expression of certain antimicrobial peptides (AMPs) [61]. There are seven specific AMPs identified in D. melanogaster: Drosomycin, Metchnikowin, Diptericin, Drosocin, Cecropin, Defensin, and Attacin [62]. Cecropin, Diptericin, Drosocin, Attacin, and Defensin are involved during bacterial infection, whereas Drosomycin and Cecropin are involved during fungal infection. Metchnikowin is involved in both forms of infection [63, 64]. These peptides are secreted into the hemolymph for antibacterial and antifungal defense.
\n
Recently, Toll was found to elicit an antiviral response (\nFigure 1\n). A Dif1\n fly mutant, which did not have a functional Toll pathway, developed higher DXV viral titers and higher mortality when compared to wild‐type flies. A gain‐of‐function Toll mutant, Tl1°b, developed a reduced DXV viral titer [65]. These results indicate that Toll may be involved in reducing viral replication of DXV and potentially other viral pathogens and warrants further characterization.
\n
Another pathway involved in antibacterial defense is Imd. Imd has a similar mechanism as Toll but targets Gram‐negative bacteria (\nFigure 1\n). The PAMPs for Gram‐negative bacteria are diaminopimelic‐containing peptidoglycan (DAP‐type PGN), which are recognized by the PRRs, PGRP‐LC, and PGRP‐LE. This triggers the Imd intracellular signaling cascade [58]. The signaling cascade activates an NF‐kB‐like factor, Relish (Rel). The Rel domain of Relish translocates to the nucleus, binds to the kB site, and induces transcription of AMPs, regulating expression [3]. Imd and Toll share the same target genes but are activated by different pathogens. In addition, Toll and Imd interact with each other to regulate a coordinated and effective immune response.
\n
The Imd pathway is implicated in an antiviral response in D. melanogaster (\nFigure 1\n). Loss‐of‐function mutant flies were created for different Imd pathways genes, such as Rel and PGRP‐LC. These flies displayed increased sensitivity to CrPV and had higher viral loads than the controls [8]. The results indicate that Imd signaling may be involved in antiviral innate immune responses during CrPV infection and requires further research.
\n
The JAK/STAT pathway is also involved in the D. melanogaster immune response (\nFigure 1\n). This pathway contributes to a systemic immune response, antiviral response, and regeneration of gut epithelium [52, 66, 67]. JAK/STAT consists of cytokine‐like molecules Unpaired (Upd) and the Upd receptor Domeless (Dome), Hopscotch (Hop), the D. melanogaster homolog of vertebrate JAK, the signal transducer and activator of transcription protein at 92E (STAT92E), and suppressors of cytokine signaling (SOC3S6E) [4, 68, 69, 70, 71, 72]. For activation of the JAK/STAT pathway, Upd binds to Dome. This binding causes Hop to phosphorylate itself and the cytoplasmic tail of Dome [68, 72]. Phosphorylation of Dome allows for the binding of STAT92E proteins. STAT92E is phosphorylated, dimerized, and translocated to the nucleus where it binds and activates transcription. SOCS36E is a negative regulator of the JAK/STAT pathway. It inhibits activation by binding the JAK complex, preventing autophosphorylation [69, 71]. JAK/STAT is also implicated in antibacterial and/or antifungal defense, but its role in antiviral defense needs further investigation.
\n
\n
\n
5. Conclusion
\n
Viral pathogens infect all organisms, including insects. For successful infection, viruses must be able to replicate and evade host immunity. D. melanogaster must rely on innate immunity to combat infection. Viral infections are easily controlled and can develop a persistent infection with no apparent pathogenesis. However, this regulation of infection is poorly understood. An uncharacterized antiviral mechanism must exist, which may include Vago, but further research is needed. A better understanding of antiviral immunity is important because many of the factors and pathways are conserved among species. Further research with viruses, especially new viruses, will help promote a better understanding of host immunity to pathogen interactions.
\n
\n
Acknowledgments
\n
The financial support was provided by grants from the National Center for Research Resources (NCRR; 5P20RR016469) and the National Institute of General Medical Science (NIGMS; 8P20GM103427), a component of the National Institutes of Health (NIH). This publication’s contents are the sole responsibility of the authors and do not necessarily represent the official views of the NIH or NIGMS.
\n
\n',keywords:"antiviral immunity, autophagy, innate immunity, RNAi, virus",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/55560.pdf",chapterXML:"https://mts.intechopen.com/source/xml/55560.xml",downloadPdfUrl:"/chapter/pdf-download/55560",previewPdfUrl:"/chapter/pdf-preview/55560",totalDownloads:818,totalViews:400,totalCrossrefCites:1,totalDimensionsCites:2,hasAltmetrics:0,dateSubmitted:"November 28th 2016",dateReviewed:"April 18th 2017",datePrePublished:"December 20th 2017",datePublished:"February 28th 2018",dateFinished:null,readingETA:"0",abstract:"The fruit fly, Drosophila melanogaster, is an extremely useful model to study innate immunity mechanisms. A fundamental understanding of these mechanisms as they relate to various pathogens has come to light over the past 30 years. The discovery of Toll‐like receptors and their recognition of shared molecules (pathogen‐associated molecular patterns or PAMPs) among pathogenic bacteria were the first detailed set of receptors to be described that act in innate immunity. The immune deficiency pathway (Imd) described in D. melanogaster functions in a very similar way to the Toll pathway in recognizing PAMPs primarily from Gram‐negative bacteria. The discovery of small interfering RNAs (RNAi) provided a means by which antiviral immunity was accomplished in invertebrates. Another related pathway, the JAK/STAT pathway, functions in a similar manner to the interferon pathways described in vertebrates, also providing antiviral defense. Recently, autophagy was also shown to function as a protective pathway against virus infection in D. melanogaster. At least three of these pathways (Imd, JAK/STAT, and RNAi) show signal integration in response to viral infection, demonstrating a coordinated immune response against viral infection. The number of pathways and the integration of them reflect the diversity of pathogens to which innate immune mechanisms must be able to respond. The viral pathogens that infect invertebrates have developed countermeasures to some of these pathways, in particular to RNAi. The evolutionary arms race of pathogen vs. host is ever ongoing.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/55560",risUrl:"/chapter/ris/55560",book:{slug:"drosophila-melanogaster-model-for-recent-advances-in-genetics-and-therapeutics"},signatures:"Wilfredo A. Lopez, Alexis M. Page, Brad L. Ericson, Darby J. Carlson\nand Kimberly A. Carlson",authors:[{id:"202812",title:"Dr.",name:"Kimberly",middleName:null,surname:"Carlson",fullName:"Kimberly Carlson",slug:"kimberly-carlson",email:"carlsonka1@unk.edu",position:null,institution:{name:"University of Nebraska at Kearney",institutionURL:null,country:{name:"United States of America"}}},{id:"202815",title:"Mr.",name:"Wilfredo",middleName:null,surname:"Lopez",fullName:"Wilfredo Lopez",slug:"wilfredo-lopez",email:"lopezwa@lopers.unk.edu",position:null,institution:null},{id:"202817",title:"Ms.",name:"Alexis",middleName:null,surname:"Page",fullName:"Alexis Page",slug:"alexis-page",email:"pageam@lopers.unk.edu",position:null,institution:null},{id:"202818",title:"Dr.",name:"Brad",middleName:null,surname:"Ericson",fullName:"Brad Ericson",slug:"brad-ericson",email:"ericsonb@unk.edu",position:null,institution:null},{id:"202819",title:"Mr.",name:"Darby",middleName:null,surname:"Carlson",fullName:"Darby Carlson",slug:"darby-carlson",email:"carlsondj@unk.edu",position:null,institution:null}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_1_2",title:"1.1. The fruit fly, Drosophila melanogaster, as a model for innate immunity",level:"2"},{id:"sec_2_2",title:"1.2. Drosophila viruses",level:"2"},{id:"sec_3_2",title:"1.3. Non‐Drosophila viruses",level:"2"},{id:"sec_5",title:"2. RNA interference (RNAi) and the immune response",level:"1"},{id:"sec_5_2",title:"2.1. Antiviral RNAi in D. melanogaster\n",level:"2"},{id:"sec_6_2",title:"2.2. Viral suppression of RNAi",level:"2"},{id:"sec_7_2",title:"2.3. Vago acts as an RNAi‐independent antiviral mechanism",level:"2"},{id:"sec_9",title:"3. Autophagy",level:"1"},{id:"sec_9_2",title:"3.1. Antiviral autophagy",level:"2"},{id:"sec_11",title:"4. Other antiviral response pathways",level:"1"},{id:"sec_12",title:"5. Conclusion",level:"1"},{id:"sec_13",title:"Acknowledgments",level:"1"}],chapterReferences:[{id:"B1",body:'\nIwasaki A, Medzhitov R. Control of adaptive immunity by the innate immune system. Nature Immunology. 2015;16(4):343-353. 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Natural selection of mutants of vesicular stomatitis virus by cultured cells of Drosophila melanogaster. Journal of General Virology. 1973;20(3):341-351. DOI: 10.1099/0022-1317‐20‐3‐341\n'},{id:"B40",body:'\nWyers FR, Richard‐Molard C, Blondel D, Dezelee S. Vesicular stomatitis virus growth in Drosophila melanogaster cells: G protein deficiency. Journal of Virology. 1980;33(1):411-422\n'},{id:"B41",body:'\nJakob NJ, Müller K, Bahr U, Darai G. Analysis of the first complete DNA sequence of an invertebrate iridovirus: Coding strategy of the genome of Chilo iridescent virus. Virology. 2001;286(1):182-196. DOI: 10.1006/viro.2001.0963\n'},{id:"B42",body:'\nEaton HE, Metcalf J, Penny E, Tcherepanov V, Upton C, Brunetti CR. Comparative genomic analysis of the family Iridoviridae: Re‐annotating and defining the core set of iridovirus genes. Virology Journal. 2007;4(1):1. DOI: 10.1186/1743‐422X‐4‐11\n'},{id:"B43",body:'\nLiu Y, Ye X, Jiang F, Liang C, Chen D, Peng J. et al. C3PO, an endoribonuclease that promotes RNAi by facilitating RISC activation. Science. 2009;325(5941):750-753. DOI: 10.1126/science.1176325\n'},{id:"B44",body:'\nOkamura K, Ishizuka A, Siomi H, Siomi MC. Distinct roles for Argonaute proteins in small RNA‐directed RNA cleavage pathways. Genes & Development. 2004;18(14):1655-1666. DOI: 10.1101/gad.1210204\n'},{id:"B45",body:'\nOlivieri D, Sykora MM, Sachidanandam R, Mechtler K, Brennecke J. An in vivo RNAi assay identifies major genetic and cellular requirements for primary piRNA biogenesis in Drosophila. The EMBO Journal. 2010;29(19):3301-3317. DOI: 10.1038/emboj.2010.212\n'},{id:"B46",body:'\nVan Mierlo JT, Bronkhorst AW, Overheul GJ, Sadanandan SA, Ekström JO, Heestermans M. et al. Convergent evolution of argonaute‐2 slicer antagonism in two distinct insect RNA viruses. PLoS Pathogens. 2012;8(8):e1002872. DOI: 10.1371/journal.ppat.1002872\n'},{id:"B47",body:'\nAliyari R, Wu Q, Li HW, Wang XH, Li F, Green LD. et al. Mechanism of induction and suppression of antiviral immunity directed by virus‐derived small RNAs in Drosophila. Cell Host & Microbe. 2008;4(4):387-397. DOI: 10.1016/j.chom.2008.09.001\n'},{id:"B48",body:'\nBronkhorst AW, van Cleef KW, Venselaar H, van Rij RP. A dsRNA‐binding protein of a complex invertebrate DNA virus suppresses the Drosophila RNAi response. Nucleic Acids Research. 2014;42(19):12237-12248. DOI: 10.1093/nar/gku910\n'},{id:"B49",body:'\nParadkar PN, Trinidad L, Voysey R, Duchemin JB, Walker PJ. Secreted Vago restricts West Nile virus infection in Culex mosquito cells by activating the JAK/STAT pathway. Proceedings of the National Academy of Sciences of the United States of America. 2012;109(46):18915-18920. DOI: 10.1073/pnas.1205231109\n'},{id:"B50",body:'\nCordes EJ, Licking‐Murray KD, Carlson KA. Differential gene expression related to Nora virus infection of Drosophila melanogaster. Virus Research. 2013;175(2):95-100. DOI: 10.1016/j.virusres.2013.03.021\n'},{id:"B51",body:'\nDeddouche S, Matt N, Budd A, Mueller S, Kemp C, Galiana‐Arnoux D. et al. The DExD/H‐box helicase Dicer‐2 mediates the induction of antiviral activity in Drosophila. Nature Immunology. 2008;9(12):1425-1432. DOI: 10.1038/ni.1664\n'},{id:"B52",body:'\nDostert C, Jouanguy E, Irving P, Troxler L, Galiana‐Arnoux D, Hetru C. et al. The JAK/STAT signaling pathway is required but not sufficient for the antiviral response of Drosophila. Nature Immunology. 2005;6(9):946-953. DOI: 10.1038/ni1237\n'},{id:"B53",body:'\nYoneyama M, Kikuchi M, Matsumoto K, Imaizumi T, Miyagishi M, Taira K. et al. Shared and unique functions of the DExD/H‐box helicases RIG‐I, MDA5, and LGP2 in antiviral innate immunity. The Journal of Immunology. 2005;175(5):2851-2858. DOI: 10.4049/jimmunol.175.5.2851\n'},{id:"B54",body:'\nParadkar PN, Duchemin JB, Voysey R, Walker PJ. Dicer‐2‐dependent activation of Culex Vago occurs via the TRAF‐Rel2 signaling pathway. PLoS Neglected Tropical Diseases. 2014;8(4):e2823. DOI: 10.1371/journal.pntd.0002823\n'},{id:"B55",body:'\nBerry DL, Baehrecke EH. Growth arrest and autophagy are required for salivary gland cell degradation in Drosophila. Cell. 2007;131(6):1137-1148. DOI: 10.1016/j.cell.2007.10.048\n'},{id:"B56",body:'\nKlionsky DJ, Emr SD. Autophagy as a regulated pathway of cellular degradation. Science. 2000;290(5497):1717-1721. DOI: 10.1126/science.290.5497.1717\n'},{id:"B57",body:'\nShelly S, Lukinova N, Bambina S, Berman A, Cherry S. Autophagy is an essential component of Drosophila immunity against vesicular stomatitis virus. Immunity. 2009;30(4):588-598. DOI: 10.1016/j.immuni.2009.02.009\n'},{id:"B58",body:'\nChamy LE, Leclerc V, Caldelari I, Reichhart J‐M. Danger signal and PAMP sensing define binary signaling pathways upstream of Toll. Nature Immunology. 2008;9(10):1165-1170. DOI: 10.1038/ni.1643\n'},{id:"B59",body:'\nGottar M, Gobert V, Matskevich AA, Reichhart JM, Wang C, Butt TM. et al. Dual detection of fungal infections in Drosophila via recognition of glucans and sensing of virulence factors. Cell. 2006;127(7):1425-1437. DOI: 10.1016/j.cell.2006.10.046\n'},{id:"B60",body:'\nJang IH, Chosa N, Kim SH, Nam HJ, Lemaitre B, Ochiai M. et al. A Spätzle‐processing enzyme required for toll signaling activation in Drosophila innate immunity. Developmental Cell. 2006;10(1):45-55. DOI: 10.1016/j.devcel.2005.11.013\n'},{id:"B61",body:'\nKanoh H, Kuraishi T, Tong LL, Watanabe R, Nagata S, Kurata S. Ex vivo genome‐wide RNAi screening of the Drosophila Toll signaling pathway elicited by a larva‐derived tissue extract. Biochemical and Biophysical Research Communications. 2015;467(2):400-406. DOI: 10.1016/j.bbrc.2015.09.138\n'},{id:"B62",body:'\nRutschmann S, Jung AC, Hetru C, Reichhart JM, Hoffmann JA, Ferrandon D. The Rel protein DIF mediates the antifungal but not the antibacterial host defense in Drosophila. Immunity. 2000;12(5):569-580. DOI: 10.1016/S1074‐7613(00)80208‐3\n'},{id:"B63",body:'\nLemaitre B, Nicolas E, Michaut L, Reichhart JM, Hoffmann JA. The dorsoventral regulatory gene cassette spätzle/Toll/cactus controls the potent antifungal response in Drosophila adults. Cell. 1996;86(6):973-983. DOI: 10.1016/S0092‐8674(00)80172‐5\n'},{id:"B64",body:'\nLemaitre B, Reichart JM, Hoffmann JA. Drosophila host defense: Differential induction of antimicrobial peptide genes after infection by various classes of microorganisms. Proceedings of the National Academy of Sciences of the United States of America. 1997;94(26):14614-14619\n'},{id:"B65",body:'\nZambon RA, Nandakumar M, Vakharia VN, Wu LP. The Toll pathway is important for an antiviral response in Drosophila. Proceedings of the National Academy of Sciences of the United States of America. 2005;102(20):7257-7262. DOI: 10.1073/pnas.0409181102\n'},{id:"B66",body:'\nYang H, Kronhamn J, Ekström JO, Korkut GG, Hultmark D. JAK/STAT signaling in Drosophila muscles controls the cellular immune response against parasitoid infection. EMBO Reports. 2015;16(12):1664-1672. DOI: 10.15252/embr.201540277\n'},{id:"B67",body:'\nJiang H, Patel PH, Kohlmaier A, Grenley MO, McEwen DG, Edgar BA. Cytokine/Jak/Stat signaling mediates regeneration and homeostasis in the Drosophila midgut. Cell. 2009;137:1343-1355. DOI: 10.1016/j.cell.2009.05.014\n'},{id:"B68",body:'\nBinari R, Perrimon N. Stripe‐specific regulation of pair‐rule genes by hopscotch, a putative Jak family tyrosine kinase in Drosophila. Genes & Development. 1994;8(3):300-312. DOI: 10.1101/gad.8.3.300\n'},{id:"B69",body:'\nYan R, Small S, Desplan C, Dearolf CR, Darnell JE. Identification of a Stat gene that functions in Drosophila development. Cell. 1996;84(3):421-430. DOI: 10.1016/S0092‐8674(00)81287‐8\n'},{id:"B70",body:'\nHarrison DA, McCoon PE, Binari R, Gilman M, Perrimon N. Drosophila unpaired encodes a secreted protein that activates the JAK signaling pathway. Genes & Development. 1998;12(20):3252-3263. DOI: 10.1101/gad.12.20.3252\n'},{id:"B71",body:'\nZeidler MP, Bach EA, Perrimon N. The roles of the Drosophila JAK/STAT pathway. Oncogene. 2000;19(21):2598-2606. DOI: 10.1038/sj.onc.1203482\n'},{id:"B72",body:'\nBrown S, Hu N, Hombriá JC. Identification of the first invertebrate interleukin JAK/STAT receptor, the Drosophila gene domeless. Current Biology. 2001;21:1700-1705. DOI: 10.1016/S0960‐9822(01)00524‐3\n'},{id:"B73",body:'\nThomas‐Orillard M. Modifications of mean ovariole number, fresh weight of adult females and developmental time in Drosophila melanogaster induced by Drosophila C virus. Genetics. 1984;107(4):635-644\n'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Wilfredo A. Lopez",address:"carlsonka1@unk.edu",affiliation:'
Department of Biology, University of Nebraska at Kearney, Kearney, Nebraska, USA
'},{corresp:null,contributorFullName:"Alexis M. Page",address:null,affiliation:'
Department of Biology, University of Nebraska at Kearney, Kearney, Nebraska, USA
'},{corresp:null,contributorFullName:"Brad L. Ericson",address:null,affiliation:'
Department of Biology, University of Nebraska at Kearney, Kearney, Nebraska, USA
'},{corresp:null,contributorFullName:"Darby J. Carlson",address:null,affiliation:'
Department of Biology, University of Nebraska at Kearney, Kearney, Nebraska, USA
'},{corresp:null,contributorFullName:"Kimberly A. Carlson",address:null,affiliation:'
Department of Biology, University of Nebraska at Kearney, Kearney, Nebraska, USA
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Carlson",authors:[{id:"202812",title:"Dr.",name:"Kimberly",middleName:null,surname:"Carlson",fullName:"Kimberly Carlson",slug:"kimberly-carlson"},{id:"202815",title:"Mr.",name:"Wilfredo",middleName:null,surname:"Lopez",fullName:"Wilfredo Lopez",slug:"wilfredo-lopez"},{id:"202817",title:"Ms.",name:"Alexis",middleName:null,surname:"Page",fullName:"Alexis Page",slug:"alexis-page"},{id:"202818",title:"Dr.",name:"Brad",middleName:null,surname:"Ericson",fullName:"Brad Ericson",slug:"brad-ericson"},{id:"202819",title:"Mr.",name:"Darby",middleName:null,surname:"Carlson",fullName:"Darby Carlson",slug:"darby-carlson"}]}]},relatedBooks:[{type:"book",id:"843",title:"Insecticides",subtitle:"Pest Engineering",isOpenForSubmission:!1,hash:"88f3cc3c937f853057f544c152ef7491",slug:"insecticides-pest-engineering",bookSignature:"Farzana Perveen",coverURL:"https://cdn.intechopen.com/books/images_new/843.jpg",editedByType:"Edited by",editors:[{id:"75563",title:"Dr.",name:"Farzana Khan",surname:"Perveen",slug:"farzana-khan-perveen",fullName:"Farzana Khan Perveen"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"},chapters:[{id:"28254",title:"Insecticide",slug:"insecticide",signatures:"A. 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Rajini",authors:[{id:"75118",title:"Dr.",name:"Padmanabhan",middleName:null,surname:"Rajini",fullName:"Padmanabhan Rajini",slug:"padmanabhan-rajini"},{id:"83243",title:"Dr.",name:"Apurva Kumar",middleName:"Ramesh",surname:"Joshi",fullName:"Apurva Kumar Joshi",slug:"apurva-kumar-joshi"}]},{id:"28257",title:"The Toxicity of Fenitrothion and Permethrin",slug:"the-toxicity-of-fenitrothion-and-permethrin",signatures:"Dong Wang, Hisao Naito and Tamie Nakajima",authors:[{id:"71957",title:"Prof.",name:"Tamie",middleName:null,surname:"Nakajima",fullName:"Tamie Nakajima",slug:"tamie-nakajima"},{id:"83511",title:"MSc.",name:"Dong",middleName:null,surname:"Wang",fullName:"Dong Wang",slug:"dong-wang"},{id:"83512",title:"Dr.",name:"Hisao",middleName:null,surname:"Naito",fullName:"Hisao Naito",slug:"hisao-naito"}]},{id:"28258",title:"DDT and Its Metabolites in Mexico",slug:"ddt-and-its-metabolites-in-mexico",signatures:"Iván Nelinho Pérez Maldonado, Jorge Alejandro Alegría-Torres, Octavio Gaspar-Ramírez, Francisco Javier Pérez Vázquez, Sandra Teresa Orta-Garcia and Lucia Guadalupe Pruneda Álvarez",authors:[{id:"75051",title:"Dr.",name:"Ivan Nelinho",middleName:null,surname:"Perez-Maldonado",fullName:"Ivan Nelinho Perez-Maldonado",slug:"ivan-nelinho-perez-maldonado"},{id:"82902",title:"MSc.",name:"Lucia Guadalupe",middleName:null,surname:"Pruneda Alvarez",fullName:"Lucia Guadalupe Pruneda Alvarez",slug:"lucia-guadalupe-pruneda-alvarez"},{id:"82905",title:"MSc.",name:"Francisco Javier",middleName:null,surname:"Perez Vazquez",fullName:"Francisco Javier Perez Vazquez",slug:"francisco-javier-perez-vazquez"},{id:"122335",title:"Dr.",name:"Jorge Alejandro",middleName:null,surname:"Alegría-Torres",fullName:"Jorge Alejandro Alegría-Torres",slug:"jorge-alejandro-alegria-torres"},{id:"122336",title:"Dr.",name:"Octavio",middleName:null,surname:"Gaspar-Ramírez",fullName:"Octavio Gaspar-Ramírez",slug:"octavio-gaspar-ramirez"},{id:"122337",title:"Dr.",name:"Sandra Teresa",middleName:null,surname:"Orta-García",fullName:"Sandra Teresa Orta-García",slug:"sandra-teresa-orta-garcia"}]},{id:"28259",title:"Presence of Dichlorodiphenyltrichloroethane (DDT) in Croatia and Evaluation of Its Genotoxicity",slug:"presence-of-dichlorodiphenyltrichloroethane-ddt-in-croatia-and-evaluation-of-its-genotoxicity",signatures:"Goran Gajski, Marko Gerić, Sanda Ravlić, Željka Capuder and Vera Garaj-Vrhovac",authors:[{id:"81623",title:"Prof.",name:"Vera",middleName:null,surname:"Garaj-Vrhovac",fullName:"Vera Garaj-Vrhovac",slug:"vera-garaj-vrhovac"},{id:"120390",title:"Dr.",name:"Goran",middleName:null,surname:"Gajski",fullName:"Goran Gajski",slug:"goran-gajski"},{id:"120391",title:"Mr.",name:"Marko",middleName:null,surname:"Gerić",fullName:"Marko Gerić",slug:"marko-geric"},{id:"120392",title:"Ms.",name:"Sanda",middleName:null,surname:"Ravlić",fullName:"Sanda Ravlić",slug:"sanda-ravlic"},{id:"120393",title:"MSc.",name:"Željka",middleName:null,surname:"Capuder",fullName:"Željka Capuder",slug:"zeljka-capuder"}]},{id:"28260",title:"Vector Control Using Insecticides",slug:"vector-control-using-insecticides",signatures:"Alhaji Aliyu",authors:[{id:"73998",title:"Dr.",name:"Alhaji",middleName:null,surname:"Aliyu",fullName:"Alhaji Aliyu",slug:"alhaji-aliyu"}]},{id:"28261",title:"Susceptibility Status of Aedes aegypti to Insecticides in Colombia",slug:"susceptibility-status-of-aedes-aegypti-to-insecticides-in-colombia",signatures:"Ronald Maestre Serrano",authors:[{id:"86194",title:"Dr.",name:"Ronald",middleName:"Yesid",surname:"Maestre Serrano",fullName:"Ronald Maestre Serrano",slug:"ronald-maestre-serrano"}]},{id:"28262",title:"Behavioral Responses of Mosquitoes to Insecticides",slug:"behavioral-responses-of-mosquitoes-to-insecticides",signatures:"Theeraphap Chareonviriyaphap",authors:[{id:"75315",title:"Prof.",name:"Theeraphap",middleName:null,surname:"Chareonviriyaphap",fullName:"Theeraphap Chareonviriyaphap",slug:"theeraphap-chareonviriyaphap"}]},{id:"28263",title:"Essential Plant Oils and Insecticidal Activity in Culex quinquefasciatus",slug:"essential-plant-oils-and-insecticidal-activity-in-culex-quinquefasciatus",signatures:"Maureen Leyva, Olinka Tiomno, Juan E. Tacoronte, Maria del Carmen Marquetti and Domingo Montada",authors:[{id:"71668",title:"MSc.",name:"Maureen",middleName:null,surname:"Leyva",fullName:"Maureen Leyva",slug:"maureen-leyva"}]},{id:"28264",title:"Biological Control of Mosquito Larvae by Bacillus thuringiensis subsp. israelensis",slug:"biological-control-of-mosquito-larvae-by-bacillus-thuringiensis-subsp-israelensis",signatures:"Mario Ramírez-Lepe and Montserrat Ramírez-Suero",authors:[{id:"76645",title:"Dr.",name:"Mario",middleName:null,surname:"Ramirez-Lepe",fullName:"Mario Ramirez-Lepe",slug:"mario-ramirez-lepe"},{id:"80064",title:"Dr.",name:"Montserrat",middleName:null,surname:"Ramirez-Suero",fullName:"Montserrat Ramirez-Suero",slug:"montserrat-ramirez-suero"}]},{id:"28265",title:"Metabolism of Pyrethroids by Mosquito Cytochrome P450 Enzymes: Impact on Vector Control",slug:"metabolism-of-pyrethroids-by-mosquito-cytochrome-p450-enzymes-impact-on-vector-control",signatures:"Pornpimol Rongnoparut, Sirikun Pethuan, Songklod Sarapusit and Panida Lertkiatmongkol",authors:[{id:"75411",title:"Dr.",name:"Pornpimol",middleName:null,surname:"Rongnoparut",fullName:"Pornpimol Rongnoparut",slug:"pornpimol-rongnoparut"}]},{id:"28266",title:"Bioactive Natural Products from Sapindaceae Deterrent and Toxic Metabolites Against Insects",slug:"bioactive-natural-products-from-sapindacea-deterrent-and-toxic-metabolites-against-insects",signatures:"Martina Díaz and Carmen Rossini",authors:[{id:"79516",title:"Dr",name:"Carmen",middleName:null,surname:"Rossini",fullName:"Carmen Rossini",slug:"carmen-rossini"},{id:"80879",title:"Prof.",name:"Martina",middleName:null,surname:"Díaz",fullName:"Martina Díaz",slug:"martina-diaz"}]},{id:"28267",title:"Pest Management Strategies for Potato Insect Pests in the Pacific Northwest of the United States",slug:"pest-management-strategies-for-potato-insect-pests-in-the-pacific-northwest-of-the-united-states",signatures:"Silvia I. Rondon",authors:[{id:"85253",title:"Dr.",name:"Silvia",middleName:null,surname:"Rondon",fullName:"Silvia Rondon",slug:"silvia-rondon"}]},{id:"28268",title:"Management of Tuta absoluta (Lepidoptera, Gelechiidae) with Insecticides on Tomatoes",slug:"management-of-tuta-absoluta-lepidoptera-gelechiidae-with-insecticides-on-tomatoes",signatures:"Mohamed Braham and Lobna Hajji",authors:[{id:"71634",title:"Dr.",name:"Mohamed",middleName:null,surname:"Braham",fullName:"Mohamed Braham",slug:"mohamed-braham"}]},{id:"28269",title:"Management Strategies for Western Flower Thrips and the Role of Insecticides",slug:"management-strategies-for-western-flower-thrips-and-the-role-of-insecticides",signatures:"Stuart R. Reitz and Joe Funderburk",authors:[{id:"77440",title:"Dr.",name:"Stuart",middleName:null,surname:"Reitz",fullName:"Stuart Reitz",slug:"stuart-reitz"},{id:"83482",title:"Dr.",name:"Joe",middleName:null,surname:"Funderburk",fullName:"Joe Funderburk",slug:"joe-funderburk"}]},{id:"28270",title:"The Past and Present of Pear Protection Against the Pear Psylla, Cacopsylla pyri L.",slug:"the-past-and-present-of-pear-protection-against-the-pear-psylla-cacopsylla-pyri-l-",signatures:"Stefano Civolani",authors:[{id:"73950",title:"Dr.",name:"Stefano",middleName:null,surname:"Civolani",fullName:"Stefano Civolani",slug:"stefano-civolani"}]},{id:"28271",title:"Effects of Kaolin Particle Film and Imidacloprid on Glassy-Winged Sharpshooter (Homalodisca vitripennis ) (Hemiptera: Cicadellidae) Populations and the Prevention of Spread of Xylella fastidiosa in Grape",slug:"effects-of-kaolin-particle-film-and-imidacloprid-on-glassy-winged-sharpshooter-homalodisca-vitripenn",signatures:"K.M. Tubajika, G.J. Puterka, N.C. Toscano, J. Chen and E.L. Civerolo",authors:[{id:"76412",title:"Dr",name:"Kayimbi",middleName:null,surname:"Tubajika",fullName:"Kayimbi Tubajika",slug:"kayimbi-tubajika"},{id:"82246",title:"Dr.",name:"Gary",middleName:null,surname:"Puterka",fullName:"Gary Puterka",slug:"gary-puterka"},{id:"90372",title:"Prof.",name:"Nick",middleName:null,surname:"Toscano",fullName:"Nick Toscano",slug:"nick-toscano"},{id:"109426",title:"Dr.",name:"Jianchi",middleName:null,surname:"Chen",fullName:"Jianchi Chen",slug:"jianchi-chen"},{id:"109427",title:"Dr.",name:"Edwin",middleName:null,surname:"Civerolo",fullName:"Edwin Civerolo",slug:"edwin-civerolo"}]},{id:"28272",title:"Use and Management of Pesticides in Small Fruit Production",slug:"use-and-management-of-pesticides-in-small-fruit-production",signatures:"Carlos García Salazar, Anamaría Gómez Rodas and John C. Wise",authors:[{id:"75562",title:"Dr",name:"Carlos",middleName:null,surname:"Garcia-Salazar",fullName:"Carlos Garcia-Salazar",slug:"carlos-garcia-salazar"}]},{id:"28273",title:"The Conundrum of Chemical Boll Weevil Control in Subtropical Regions",slug:"the-conundrum-of-chemical-boll-weevil-control-in-subtropical-regions",signatures:"Allan T. Showler",authors:[{id:"72273",title:"Dr.",name:"Allan T.",middleName:null,surname:"Showler",fullName:"Allan T. Showler",slug:"allan-t.-showler"}]},{id:"28274",title:"Management of Tsetse Fly Using Insecticides in Northern Botswana",slug:"management-of-tsetse-fly-using-insecticides-in-northern-botswana",signatures:"C. N. Kurugundla, P. M. Kgori and N. Moleele",authors:[{id:"73921",title:"Dr.",name:"Chandrasekar Naidu",middleName:null,surname:"Kurugundla",fullName:"Chandrasekar Naidu Kurugundla",slug:"chandrasekar-naidu-kurugundla"},{id:"83853",title:"MSc.",name:"Patrick",middleName:"Mokula",surname:"Kgori",fullName:"Patrick Kgori",slug:"patrick-kgori"},{id:"83856",title:"Dr.",name:"Nkobi",middleName:null,surname:"Moleele",fullName:"Nkobi Moleele",slug:"nkobi-moleele"}]},{id:"28275",title:"Trends in Insecticide Resistance in Natural Populations of Malaria Vectors in Burkina Faso, West Africa: 10 Years’ Surveys",slug:"trends-in-insecticide-resistance-in-natural-populations-of-malaria-vectors-in-burkina-faso-west-afri",signatures:"K. R. Dabiré, A. Diabaté, M. Namountougou, L. Djogbenou, C. Wondji, F. Chandre, F. Simard, J-B. Ouédraogo, T. Martin, M. Weill and T. Baldet",authors:[{id:"75213",title:"Dr.",name:"Kounbobr Roch",middleName:null,surname:"Dabiré",fullName:"Kounbobr Roch Dabiré",slug:"kounbobr-roch-dabire"},{id:"140689",title:"Dr.",name:"Abdoulaye",middleName:null,surname:"Diabate",fullName:"Abdoulaye Diabate",slug:"abdoulaye-diabate"},{id:"140690",title:"Dr.",name:"Moussa",middleName:null,surname:"Namountougou",fullName:"Moussa Namountougou",slug:"moussa-namountougou"},{id:"140691",title:"Dr.",name:"Luc",middleName:null,surname:"Djogbenou",fullName:"Luc Djogbenou",slug:"luc-djogbenou"},{id:"140692",title:"Dr.",name:"Charles S.",middleName:null,surname:"Wondji",fullName:"Charles S. Wondji",slug:"charles-s.-wondji"},{id:"140693",title:"Dr.",name:"Fabrice",middleName:null,surname:"Chandre",fullName:"Fabrice Chandre",slug:"fabrice-chandre"},{id:"140694",title:"Dr.",name:"Frédéric",middleName:null,surname:"Simard",fullName:"Frédéric Simard",slug:"frederic-simard"},{id:"140695",title:"Dr.",name:"Jean-Bosco",middleName:null,surname:"Ouédraogo",fullName:"Jean-Bosco Ouédraogo",slug:"jean-bosco-ouedraogo"},{id:"140696",title:"Dr.",name:"Mylène",middleName:null,surname:"Weill",fullName:"Mylène Weill",slug:"mylene-weill"},{id:"140697",title:"Dr.",name:"Thierry",middleName:null,surname:"Balder",fullName:"Thierry Balder",slug:"thierry-balder"}]},{id:"28276",title:"The Role of Anopheles gambiae P450 Cytochrome in Insecticide Resistance and Infection",slug:"the-role-of-anopheles-gambiae-p450-cytochrome-in-insecticide-resistance-and-infection",signatures:"Rute Félix and Henrique Silveira",authors:[{id:"76938",title:"Prof.",name:"Henrique",middleName:null,surname:"Silveira",fullName:"Henrique Silveira",slug:"henrique-silveira"},{id:"94186",title:"Ms.",name:"Rute",middleName:null,surname:"Felix",fullName:"Rute Felix",slug:"rute-felix"}]},{id:"28277",title:"Genetic Toxicological Profile of Carbofuran and Pirimicarb Carbamic Insecticides",slug:"genetic-toxicological-profile-of-carbofuran-and-pirimicarb-carbamic-insecticides",signatures:"Sonia Soloneski and Marcelo L. Larramendy",authors:[{id:"14764",title:"Dr.",name:"Marcelo L.",middleName:null,surname:"Larramendy",fullName:"Marcelo L. Larramendy",slug:"marcelo-l.-larramendy"},{id:"14863",title:"Dr.",name:"Sonia",middleName:null,surname:"Soloneski",fullName:"Sonia Soloneski",slug:"sonia-soloneski"}]}]}]},onlineFirst:{chapter:{type:"chapter",id:"73589",title:"Sources, Fate, and Impact of Microplastics in Aquatic Environment",doi:"10.5772/intechopen.93805",slug:"sources-fate-and-impact-of-microplastics-in-aquatic-environment",body:'\n
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1. Introduction
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Due to the permanence and robustness, plastic has infiltrated every aspect of life like in clothing, electronics, cleaning products as well as in building materials [1]. World production of synthetic organic polymer plastic has skyrocketed from 1950 to 2013, showing an escalation from 1.5 to 299 million tons. Around 8-16 million tons plastic waste invades sea and oceans annually, substantial section of which comes from land borne sources [1, 2]. In the very beginning more attentiveness was towards large plastic debris; however prevalence of smaller plastic particles in the marine environment elucidated in early 1970’s [3, 4]. Due to minuscule proportion of microplastics they are ingested by protozoans to marine mammals and by many filter feeders [5]. Amphipods, polychaete worms, barnacles and sea cucumber ingest microplastic which gets accumulated in food web [6]. According to Setälä et al. [7] and Green et al. [8] microplastics are omnipresent in nature and possess high potential to interrelate with environment (biotic and abiotic) thus menacing with biogenic domain of flora and fauna. Presences of microplastics were perceived more in aquatic ecosystems, surface waters, sediments and water column. Deep seas and mountain lakes were also sullied by the presence of microplastics and thus scrutinized as global pollutant [9, 10]. Worldwide pollution provoked by plastic is dispersed maximum across seas and oceans. Longevity and buoyancy are some properties that have led these pollutants fall under the category of hazardous waste [11, 12, 13]. In the environment microplastics are present in heterogeneous group, according to varying size and shape, specific density and composition. Prodigious plastic wastes are easily perceptible [14, 15]. Although microplastics are inconspicuous, their dissemination into the oceans has profound repercussions leading to cumulative effect in the food chain [16].
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Microplastics may pose a risk to aquatic environments due to their documented ubiquity in marine ecosystems, long residence time, and propensity to be ingested by biota. As Microplastics from different sources ultimately reaches water bodies and from here microplastics disperse into surface water, underground water, and benthic sediment, etc. and their bioavailability gets affected [17]. After consumption or ingestion, microplastics can remain in the digestive tracts of aquatic organisms for periods of days to weeks before excretion. The more time of excretion likely allows the transfer of microplastics both up the food web and to new geographic locations. Exposure of individual aquatic organisms to microplastics may negatively impact feeding, growth, reproductive capabilities, or survival [18]. While studies and reviews on plastic pollution in the marine environment are increasingly common, to date, few studies have assessed the sources, fate and impact of microplastics in freshwater as well as marine environment. Thus, the present article has been made in order to fill the lacuna in this regard.
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2. Types of microplastics
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Two primary or foremost types of microplastics are: primary and secondary microplastics. According to Sundt et al. [19] plastics that are instantaneously propagated into the environment compose primary microplastics. They are produced in relatively micro size. Secondary microplastics pioneered from the deterioration or fragmentation of larger plastics.
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2.1 Primary microplastics
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Plastic ranging between size of 1 μm and 5 mm are considered primary microplastics. Microplastics are affixed to certain products due to their discrete functions. They are also operated as mordant in cosmetics and soap products and also act as conveyor of pigments. Plastic powder, granulates, pellets are some examples of primary microplastics [1, 20]. Primary microplastics are also used as exfoliates. They are the main protagonist of several day to day products like hand cleaners, toothpastes, face washes [20]. Primary microplastics are also used in dental polishes. If they are not discarded in the efficient way possible, they end up blemishing the environment. Primary microplastics also possess diverse industrial implementations like for gas and oil analysis they are required as drilling fluids, for cleaning metal surfaces to eliminate the paint, rinsing of engines etc. [21, 22, 23]. Microplastics like polystyrene, acrylic, polyester are used in industries [24].
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2.2 Secondary microplastics
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Repudiated plastic bags or fishing nets, household items and discarded plastics undergo weathering and photo degradation process and get transfigured into smaller plastic particles, thus constituting secondary microplastics. Abrasion of plastics is manifested by UV light at soil surface and by ocean waves. Secondary microplastics are also fabricated by washing machines [24, 25]. It also includes fragments of textile fiber originated from synthetic fibers, and released during the laundering process [26]. The root sources of secondary microplastics are discarded plastic debris from household items and industrial products. Secondary microplastics are considered to be the most dominating microplastics [27, 28]. Their copiousness in water bodies increases with elevating discharge of plastic debris and its continuous transformation into secondary microplastics. Textile industry products, tires, decorative paints all contribute to the genesis of secondary microplastics [20].
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3. Sources of microplastics
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3.1 Personal care products
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According to Leslie [29] plastic microbeads are utilized as additives in countless cosmetics and personal care products. They act as sorbent as well as exfoliators. Plastic microbeads are incorporated in several cosmetic products such as 350,000 plastic particles were observed in a facial scrub tube in USA [20]. A study from USA also evaluated the presence of 1700-6400 particles of plastic per g in toothpaste [1]. According to Strand [30] toothpaste contains 0.1-0.4% microbeads in accordance with weight, facial scrubs contain around 1.6-3.0%. Facial scrub possesses 0.9-4.2%, exfoliating scrub contains 10.6% and shower gel around 0.5-3.0%. One of the plastic types that are frequently perceived in microplastics is polyethylene (PE). In European country PE plastic microbeads were considered most dominating, with around 4073 tons usage.
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3.2 Blasting abrasives and cleaning products
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For cleansing surfaces primary microplastics are used as abrasive. Plastic such as polyester, polycarbonate, polyamide is used in blast media. Main purpose of blasting abrasives is in cleansing of rims, removal of paints and cleansing of ships. These abrasives are also used in marine industries for cleaning the tanks. Blasting is done in different cabins, closed or semi-closed. Area must be encrusted properly. Emission rate are quite high if done in open premises. Turbines blades are cleansed by this process; this leads to release of primary microplastics in aquatic environment. Microplastics are even used in maintenance and cleaning products as abrasive material. To remove grease, paints, oil from hands primary microplastics are used [20].
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3.3 Synthetic textile and tyres
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Browne et al. [25] assorted that process of laundries in household and industries leads to mass production of primary microplastics via scraping and dispersion of fibers, which was then emitted out in sewage water and culminates in the ocean [31]. Tyres contain profuse mixture of several synthetic polymers in addition with natural rubber. Tyres get deteriorated when used and tyre dust that contains synthetic rubber circulated by wind or swiped away by rain. Large segments of such particles were reported to congregate in the sea [19, 23].
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3.4 Paint and wood preservatives
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Primary microplastics are appended to paint and preservative. This gives matting effect and acts as color amplifier. This improves longevity of wood, provides hardened and abrasion resistance. It is also used to diminish the density of paints [20]. A study done by Poulsen et al. [32] stated that 8-30% of waste generation is triggered by paint spillage and other paint jobs. Approximately 65-97% of waste culminates as solid waste and around 35% ended up in sewer system. 1.0-5.3 t/y is the estimated amount of microplastics release from paints, out of which 0.1-0.5 t/y is the guesstimate amount of primary microplastics in paints that ends up in aquatic environment.
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3.5 Synthetic waxes and oil-gas industry
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According to Essel et al. [23] synthetic waxes are scrutinized as primary microplastics. They are used in dyeing, food coating, as lubricants and also in processing of plastics. Synthetic waxes are also used to coat papers they are extensively operative in textile processing by providing smoother surface. Polytetrafluroethylene (PTFR) is used for drilling purpose. Drilling fluids composed of microbeads, used in oil-gas industry [19, 32]. This chemical gets directly discharge into the oceans, contributing to microplastics accumulation.
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3.6 Plastic pellets manufactures
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Pellets are the primary form of many plastics around 2.55 mm in diameter. These pellets are used to generate plastic products. These pellets, spherules contribute to 79.4% of total plastic debris in the water of river Danube [33, 34]. According to Dhodapkar et al. [35], in addition to pellets, plastic dust also gets accumulated during manufacturing process or generated due to relocation and transportation [20]. Pellets contain certain perilous additives like plasticizers and flame retardants that promote the eco toxicity. These additives mixed prior to the production or added during conversion. These pellets are often termed as nibs and nurdles [19].
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3.7 Weathering and abrasion
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Metropolitan environment often encounters with city dust. Synthetic cooking utensils abrasion, footwear soles abrasion, infrastructure abrasion, blasting abrasives all culminates into city dust. Independently importance of these factors is insignificant but together they are accountable for sizeable losses in the country [20, 31]. For the advancements of roads, road markings are administered. Thermoplastic, paint, polymer tapes are preferred in this process. Weathering by vehicles induces microplastics loss, which is washed off by rain or wind and ultimately outstretched to oceans [20]. Coatings of boats are done by various anticorrosive paints, mostly polyurethane, lacquers and vinyl [36].
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3.8 Packaging material and litter
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Higher preference is given to packaging materials as a source of microplastics. It contributes to about 62% of all plastic collected. It usually involves secondary microplastics. Plastic bags, soft drink bottles all culminates into it [1]. Packaging materials constitutes major portion of litter. Toys, cutlery, shoes, clothing are other forms of litter [15]. Litter from agricultural plastics is non-biodegradable, although biodegradable plastics are also prevalent nowadays. Addition of preservatives in such plastics make them less biodegradable, and these plastics get perished into smaller fragments, eventually via nearby streams microplastics enters surface water [1].
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3.9 Domestic items, food stuffs and toys
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According to United Nations Environment Programme (UNEP), 2014 [15], domestic items are considered as the mighty source of pollution in the sea. Items like cups, plastic cutlery, bottles and straws are present in abundance in oceans. Food stuffs and snacks also contribute to microplastics. Chewing gum contains microplastics fillers. A study done at Dutch coast revealed the presence of 105 particles of microplastics per gram in mussels and for oyster it reaches up to 87 microplastics particles per gram [37]. Party items like balloons, confetti firework wastes, fragments of toys all culminate to waterborne litter. Loom bracelets contain microplastics which can adulterate the environment via surface runoff [38].
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3.10 Medical resources
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In medical sector, microplastics are profoundly used [23]. Microplastics treat the reverse flow of gastric juices. Aluminum coated compounds tend to possess deleterious effect on human health. They are replaced by microplastics. Nappies, sanitary towels, plasters constitute litter. Capsules used in the edicine field contain plastic. Spectacles, contact lenses are one of the define sources of microplastics [1].
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4. Microplastics in marine ecosystems
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The pollution of microplastics varies geographically with location because as the consumption of plastic increases, there is increase in production of MP. Marine life is more disturbed by this plastic waste because ocean become a dump yard for running water system either directly via riverine system as river ultimately end up meet up with the ocean or indirectly as waste water treatment plant dispose of their waste directly in the ocean or in river which end up by meeting the marine water body. However, the size of sediment and distribution of MP is influenced by oxidative degradation (either photo- or thermal initiated), friction and biodegradation [39, 40]. The typical shape of microplastics consists of pellets, fibers and fragments but according to literature, majority of microplastics in Oceans are microfibers [41, 42]. Distribution and abundance of microplastics is chiefly determined by environmental [42, 43, 44] and anthropogenic factors [45]. Environmental factors include runoff, infiltration, river discharge, wind action, ocean currents, cyclones, river hydrodynamics, wave current, tides and movement/dispersion of animals. On the other hand, anthropogenic activities either they are for industrial or tourism or transport purpose which further led to accumulation of plastic debris in environment. According to literature, these environmental factors play vital role in determining the distribution of microplastics more intensely than anthropogenic activities, however anthropogenic activities are the core source of production of these plastic wastes.
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Abundance of microplastics in oceans distribute across various strata of Ocean. In the sediments- water systems, microplastics only sink and accumulate in the sediment when their density exceed seawater (>1.02 g/cm3); otherwise it tends to float on the sea surface or in the water column [46], hence low density microplastics float on surface layer of ocean water whereas high density microplastics sinks down to benthos layer [5]. Buoyancy of microplastics can depend on befouling in which former biomass accumulation led to increase in microplastics density and later can decrease microplastics density which is responsible for sinking, neutral or floating action of microplastics. But in case of High density microplastics, there distribution depends on other factors also like change in tidal fronts, high flow rates or larger surface area of High density microplastics.
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Beaches are a reservoir of highly fragmented plastic debris that transport microplastics back to costal water and finally to open ocean [47]. It is based on observation of Wang et al. [48] that concentration of microplastics is usually higher in upper layer i.e. epipelagic layer than the immediate lower mesopelagic layer this may be due to preferential flow or animal movement. Even, mesoscale ocean dynamics have impact on distribution of plastic debris at sea surface within subtropical gyres [49]. Usually, sea platforms and marine trafficking are responsible for microplastics in far off Ocean, whereas microplastics in near shore originate mostly from waste water, runoffs, rivers etc. [50, 51]. However terrestrial environment also determines the concentration of microplastics as harbor and industries add huge amount of plastic debris either directly or indirectly which add up to the acumen concentration of microplastics in the ocean. The dire situation of disturbance in aquatic ecosystem is becoming huge day by day as these not only affect flora but fauna as well; even coral beds are not far away from disturbance. This plastic debris also includes mesoplastics accumulation. Use and through plastic items are becoming huge threat to the aquatic organisms hence number of reports are increasing in this area of research which indicate the negative impact of microplastics and is alarming accumulation rate in ecosystem which is also eye catching for researchers and environmentalists.
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5. Microplastics in freshwater ecosystem
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To understand the impact of microplastics pollution in freshwater environment, various aspects are to be analyzed i.e. source, distribution, type and effect of microplastics. Source of freshwater pollution is usually synthetic textile, personal care products, industrial raw material, whereas the main source of microplastics in riverine system are wastewater discharge which may be industrial or household untreated waste water disposal. Microplastics are of serious concern because their accumulation potential increases with decreasing size [52]. It is also noted that, there may be change of composition of MP as they accumulate with waterborne contaminates which includes metals and persistent, bioaccumulative and toxic compounds this is possible due to larger surface-to-volume ratio. Studies by Engler [53] showed relationship between plastic debris and PBTs (e.g. PCBs and DDT) similarly a number of studies exist for polycyclic aromatic hydrocarbons [54, 55, 56]. Since the spectrum of contaminants is different between freshwater and marine system. In stagnant riverine system like ponds and lakes water pollution is more severe problems because of the irresponsible behavior of the inhabitants or by various tourism related activities which disturb the ecosystem due to accumulation of degradable or non- degradable waste. They float in the surface water and stay in the water sink into sediments of lake. For stagnant system rate of accumulation of microplastics is higher, since there is no efflux. Therefore, it can be concluded that there is a direct correlation between distance of contamination source and microplastics pollution levels in sediments [57]. Various studies confirmed the presence of microplastics in drinking water system which makes it a serious issue [58]. Research about river system and watersheds can provide the knowledge to the people to understand the alarming situation of microplastics accumulation in freshwater system [59]. Further the flow of river plays significant role in removal of plastic fragments. It is also observed that after precipitation high amount of MP is observed in sediments and running water [60]. Eventually, freshwater system also contributes to the pollutant content of marine ecosystems because ultimately riverine merge with the ocean resulting merger of mineral, sediments, soil content as well as pollutants. Hence the fact that freshwater system act as strong source of microplastics to marine ecosystem cannot be neglected. Although distribution of microplastics in freshwater system is not uniform, it depends on nearby source of waste water disposal.
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It is observed that the condemnation in water is observed higher in riverine near industrial area as compared to the residential area. However waste water treatment plants are established by organizations but they remove large plastic waste more efficiently than meso and micro plastic waste, as various technologies are installed to remove large size particle but these are not specified to retain microplastics [61, 62]. Discharge from waste water treatment plant contain may hazardous compounds along with micro –and Nano- plastic particles which enter the food web and cause diverse effect in biotic ecosystem.
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6. Fate of microplastics
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The threat of microplastics is rapidly increasing, and as the global plastic production projected to reach an accumulative 25 billion tons by 2050, things are going to be worse [63]. Although these plastic materials are key factors for innovation and development of various fields such as healthcare, energy generation, aerospace, automotive industries, construction, electronics, packaging, textile and many others [64]. However, instead of recycling or incineration or utilizing any other way of removing unused or discarded plastic from environment, these plastic wastes enters the environment from year to year and it is accumulated in Marine, freshwater and terrestrial ecosystem worldwide, even from densely populated countries like India and China to cold desert like Antarctica. And this became a matter of concern for scientists across the world. The reliance on plastic for huge number of consumer products, many of them being single-use, results in continuous entry into environment.
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No doubt, with due course of time via biotic and abiotic degradation pathway, plastic loose its mechanical integrity but it may take several years to degrade completely. With gradual degradation this immortal plastic emits smaller size particle in environment i.e. macroplastics, mesoplastics and microplastics. Plastic particles <5 mm size are considered Microplastic, although there are efforts to redefine them as <1 mm in size, as recommended by [65]. However minimum size of Microplastics has not yet been specified and it depends on the sampling and processing as well as on the applied method for Microplastics identification.
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7. Effect of microplastics on aquatic biota
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Microplastics are of special concern because they can be ingested throughout the food web more readily than larger particles. It is to be noted that the impact of microplastics on public health and aquatic ecosystems is not yet fully understood, but there is increasing number of reports which indicate negative impact of microplastics on marine and freshwater biota.
\n
With increased focus on microplastics debris, several groups have studied the influence of microplastics uptake by different organisms. As microplastics invasion appear to occur across all ecosystem from terrestrial to marine environment in different trophic level not only invertebrates but vertebrates also seem to be affected by their presence [66, 67]. Organism ingests these microplastics debris while swallowing their food. And with due course of time bioaccumulation of microplastics results in diverse negative impact on various organism like disruption of organ system, rupturing of digestive system, weakening of immune system, impotency, various respiratory and circulatory problems, even failure of organ and in extreme cases led to death of organism [51, 68, 69]. However, continuous accumulation of these deadly microplastics in various systems of the body is possible through food chain via ingestion as well as by accumulation around gill aperture (or around respiratory apertures) and appendages of body by diverse aquatic organisms [70, 71]. However, situation become direr for the predators and humans which directly or indirectly consume microplastics affected aquatic organisms [72]. As reported by Wright et al. [5], there are various consequences from ingestion of plastics and MPs by various species such as planktons, copepods, zooplanktons, crabs, small fishes, turtles, fish larvae, sea birds and mammals.
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7.1 Effect of microplastics on marine ecosystem
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Marine microplastics debris is a global threat because of its abundance, persistence and mobility across scale, with subsequent widespread distribution potential, geophysical and biological impact [73]. Across the globe, research on the ingestion of microplastics by biota has predominantly focused on wide range of marine species with different feeding strategies [74, 75, 76]. As microplastics have been shown to obstruct feeding appendages and limit food intake, physical injury and oxidative stress, reduced energy allocation in various aquatic organisms and in some cases damages in the alimentary canal were also observed [77]. Alteration in the feeding behavior of some group of crustaceans was also studied such as in copepods which feed on algae, but when these copepods feed on natural assemblage of algae with the addition of polystyrene microbeads they showed a significant decrease in herbivory which further results in decrease in growth rate of organism [5, 78]. However, it is not just growths which microplastics injection can disrupt, but also observable change in physical development of organism. An alternation was observed in life cycle of sea urchin Paracentrotus lividus which depicted alterations in shape of pelagic planktotrophic pluteus larva when Microplastics were ingested [79]. Another study of Kaposi et al. [80] by examining short term exposure of Polyethylene on the sea urchin Tripneustes gratilla, which was done by using fluorescent labels green PE Microspheres having diameter 10-45 μm, with exposure of time ranged between 15 min to 5 d. There was decrease in injection rate even when phytoplankton food was provided.
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While some of the chemicals associates with microplastics, which possess endocrine disruptive activity and are responsible for the hormonal imbalance in organisms [81]. In a study by Sussarellu et al. [82] on Oysters which is a keystone species with high ecological and economic value. When adult oysters were exposed to microplastics polystyrene of diameter about 2 μm during a critical point of their reproductive stage adults were preparing for production of gametes. And after the exposure, there was an alteration in the feeding as well as absorption efficiency of food. Reproductive changes were also observed that there is reduction in the quality of oocytes and sperm swimming speed as well as fecundity. Moreover, these impacts had clear carryover effect on offspring quality and further reduced growth in their larval progeny. Similar effects were observed in planktonic copepods when exposed to micropolystyrene for prolonged period followed by reduced food consumption and resulting in reduced reproductive outputs [83].
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However, Corals which occur in both deep sea and Antarctic system are not untouched by the effect of microplastics as some of the corals known to ingest microplastics and demonstrably negatively impact occurs both in terms of energy level, growth and pathogen frequency of reefs [84, 85].
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7.2 Effect of microplastics on fresh water ecosystem
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It’s is not only marine wildlife that can take up microplastics, bioavailability of microplastics for freshwater fauna (for both invertebrates and fishes) has also been observed. Although there are few freshwater studies so far, A study by Rehse et al.[86] shows that immobilization has occurred in freshwater zooplankton (Daphnia magna) after ingestion of polyethylene microplastics of about 1 mm, however due to the smaller size of this freshwater zooplankton, it was not able to engulf microplastics of more than 1 mm size. It is also observed that small size microplastics usually possess large surface area to volume ratio which differentiates the property of microplastics from meso and macroplastics.
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In freshwater habitat, the different POPs (persistent organic pollutants) that is PCBs (polychlorinated biphenyls), HCBs (hexachlorobenzenes), PBDEs (polybrominated diphenyl ethers) and metals are present in significantly higher concentrations. And the adsorption ratio of POPs to microplastics is different in freshwater as compared to marine ecosystems due to the proximity to the sources and use of these chemicals. As organism in freshwater ecosystem are more exposed to POPs and microplastics due to occurrence of industrial and populous area nearby. Study by Rochman et al. [87] revealed that freshwater fishes experience hepatic stress due to ingestion of polyethylene which ultimately led to bioaccumulation and toxicity in fishes. A significant amount of POPs to microplastics could accumulate in adult zebrafish gills and zebra fish embryos [88]. Another observation in the study of European perch Perca fluviatilis by Lönnstedt and Eklöv [89], suggested the effect of microplastics when larva of European perch were exposed to different concentrations of 10,000 or 80,000 particles/meter which resulted in inhibition of hatching and reduced growth rates. There were alterations in the feeding and innate behavior as compared to normal individuals which were not exposed with microplastics.
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Microplastics can also act as an artificial substrate for microorganisms. This has raised concern about the potential ecological effect on freshwater habitat, which is utilized for anthropogenic activities as well as by the wildlife organisms. Microplastics form biofilms by providing surface for microorganisms and rafting the colonized organisms over long distances. It has also been shown that biofilms containing potentially pathogenic microorganisms which can develop on plastic in the marine system. Some microorganisms in the biofilm are assumed to be potentially opportunistic (human) pathogens, for example, members of the genus Vibrio have been found on the particles and making microplastics vector for pathogens, toxic algae, bacteria and invasive species. Various studies are performed on different rivers for the estimation of assimilation of microplastics by aquatic organisms. A study conducted by McGoran et al. [90], in the river Thames, revealed that up to 75% of sampled European flounder (Platichthys flesus) has plastic fibers in their gut compared to 20% of European smelt (Osmeruseperlanus) however it is estimated that this huge difference in the concentration is due to the feeding habitats of both the fishes as European flounder are benthic feeders while European smelt are pelagic feeder and these observations also suggested the relative distribution of microplastics in different strata of riverine system [91].
\n
In study of microplastics in freshwater, Au et al. [92], investigated the ingestion and effects of PE (fluorescent blue PE microplastics particles, 10–27 μm) and PP (black polypropylene microplastics fibers from marine rope, 20–75 mm in length) on the growth and mortality of the freshwater amphipod Hyalella azteca. The LC50 of PE and PP in H. azteca after a 10-d exposure were 4.6 × 104 and 71 microplastics/mL respectively. The effects of chronic exposure to PE and its influence on the reproduction of amphipods were analyzed. Chronic exposure of H. azteca to PP fibers, even at a low concentration, significantly decreased growth and reproduction.
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7.3 Toxic effects of microplastics shown by trophic transfer
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To evaluate the process of trophic transfer and toxicological effects of microplastics at different trophic levels, a number of factors need to be considered that are involved in ingestion, bioaccumulation and biomagnification of microplastics and their associated chemicals.
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Resemblance in shape and size of microplastics with many species of planktons and other type of food particles is usually observed. Hence sometimes microplastics are normally ingested by aquatic filter feeders along with some associated contaminants led to bioaccumulation and trophic transfer to higher organisms [93].The size and shape of plastic particles are the two most important parameters which determine the extent of microplastics retention. This is because smaller particles are more likely to be ingested and particles with angular shapes may be harder to egest. The available body of evidence indicated that trophic transfer of microplastics may occur [94, 95]. Hence, pollutants may be transferred along with microplastics by means of oral ingestion as well as other pathways, which include ventilation or simple microplastics attachment and resuspension into the water column [88, 96].
\n
Setälä et al. [7], observed the trophic transfer of polystyrene microplastics to macrozooplankton occurred after only 3 hrs of exposure to mesozooplaktons that had previously infested PS microplastics. Studies also revealed that uptake of microplastics can be influenced by the surface characteristics of plastic particles. As MP that was neutrally or positively charged had a higher binding affinity for algal cell wall than negatively charged microplastics. And hence they adhere to surface of seaweeds like Fucus vesiculosus, resulting in their consumption by grazing gastropods which further eventually led to trophic transfer of microplastics [97]. Microplastics are ingested by organism at lower trophic level and are further transferred to higher trophic level and ultimately results in bioaccumulation in higher organism and causes ill effects which may be life threating for them.
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The impact of microplastics on humans is not yet fully understood, however many studies depict that there are many chemicals that are used in plastic production show toxic effect on living organism some of these chemicals are bisphenol A (BPA), polybrominated diphenyl ethers (PBDE), and tetrabromobisphenol (TBBPA). Studies have already detected these chemicals in human tissues and biological fluids [27]. It has also been reported that additives, for example, di(2-ethylhexyl)phthalate (DEHP), can leach from medical supplies made of PVC and accumulate in the blood of hemodialysis patients [98]. Moreover, the presence of microplastics in seafood, for example, bivalves cultured for human consumption has already been shown [28, 99]. It should be further investigated whether beverage or food products act as possible microplastics sources which is can further enter food web and results in bioaccumulation in living organism.
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8. Management of microplastics
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To get the problem under control, the society has to take initiatives which includes significantly curtailing unnecessary single-use plastic items such as water bottles, plastic shopping bags, straws and utensils, stringent policies should be implemented by the governments ensuring the need to strengthen garbage collection and recycling systems to prevent waste from leaking into the environment to improve recycling rates. New ways to break plastic down into its most basic units, which can be rebuilt into new plastics or other materials should be considered.
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9. Conclusion
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Production and applications of microplastics resulted to an enhanced incidence of plastics debris and microplastics, in the aquatic environment. Not only one mechanism such as the weathering-related fracturing and surface embrittlement of plastics in beach environments is the root cause of generation of microplastics but industrial waste also constitute the major sources of them. As microplastics are recalcitrant in nature, only small fraction of the microplastics present in aquatic body imposes a serious threat to aquatic life. As microplastics are potentially ingestible by aquatic organisms including micro and nano plankton species, the delivery of toxins across trophic levels via this mechanism is very common. The efficiency of such transfer will depend on the bioavailability of microplastics and the residence time of meso or microplastics in the organisms. Endocytosis of plastic nanoparticles by micro- or nanofauna can also result in adverse toxic endpoints. As aquatic species constitute the very foundation of the aquatic food web, any threat to these can have serious and far-reaching effects in the world oceans. There is an urgent need to quantify the magnitude of these potential outcomes and assess the future impact of increasing microplastics levels on the world’s aquatic bodies.
\n
\n\n',keywords:"microplastics, sources, accumulation, toxicity, aquatic organisms",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/73589.pdf",chapterXML:"https://mts.intechopen.com/source/xml/73589.xml",downloadPdfUrl:"/chapter/pdf-download/73589",previewPdfUrl:"/chapter/pdf-preview/73589",totalDownloads:134,totalViews:0,totalCrossrefCites:0,dateSubmitted:"July 6th 2020",dateReviewed:"August 31st 2020",datePrePublished:"October 14th 2020",datePublished:null,dateFinished:null,readingETA:"0",abstract:"Over the past decade, enhanced scientific interest has produced an expanding knowledge base for microplastics. The highest abundance of microplastics is typically associated with coastlines and oceans but the fate of these microplastics is elusive. Microplastics sink following fragmentation which is further ingested by marine biota thus imposes threat to them. Thus, the present review focuses on properties and sources of microplastics, its impact on environment, the bioaccumulation and trophic transfer of microplastics and its impact on living biota. This study would be helpful for the development and implementation of risk management strategies for managing the disposal of microplastics.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/73589",risUrl:"/chapter/ris/73589",signatures:"Sukanya Mehra, Khushboo Sharma, Geetika Sharma, Mandeep Singh and Pooja Chadha",book:{id:"10030",title:"Emerging Contaminants",subtitle:null,fullTitle:"Emerging Contaminants",slug:null,publishedDate:null,bookSignature:"Dr. Aurel Nuro",coverURL:"https://cdn.intechopen.com/books/images_new/10030.jpg",licenceType:"CC BY 3.0",editedByType:null,editors:[{id:"14427",title:"Dr.",name:"Aurel",middleName:null,surname:"Nuro",slug:"aurel-nuro",fullName:"Aurel Nuro"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:null,sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Types of microplastics",level:"1"},{id:"sec_2_2",title:"2.1 Primary microplastics",level:"2"},{id:"sec_3_2",title:"2.2 Secondary microplastics",level:"2"},{id:"sec_5",title:"3. Sources of microplastics",level:"1"},{id:"sec_5_2",title:"3.1 Personal care products",level:"2"},{id:"sec_6_2",title:"3.2 Blasting abrasives and cleaning products",level:"2"},{id:"sec_7_2",title:"3.3 Synthetic textile and tyres",level:"2"},{id:"sec_8_2",title:"3.4 Paint and wood preservatives",level:"2"},{id:"sec_9_2",title:"3.5 Synthetic waxes and oil-gas industry",level:"2"},{id:"sec_10_2",title:"3.6 Plastic pellets manufactures",level:"2"},{id:"sec_11_2",title:"3.7 Weathering and abrasion",level:"2"},{id:"sec_12_2",title:"3.8 Packaging material and litter",level:"2"},{id:"sec_13_2",title:"3.9 Domestic items, food stuffs and toys",level:"2"},{id:"sec_14_2",title:"3.10 Medical resources",level:"2"},{id:"sec_16",title:"4. Microplastics in marine ecosystems",level:"1"},{id:"sec_17",title:"5. Microplastics in freshwater ecosystem",level:"1"},{id:"sec_18",title:"6. Fate of microplastics",level:"1"},{id:"sec_19",title:"7. Effect of microplastics on aquatic biota",level:"1"},{id:"sec_19_2",title:"7.1 Effect of microplastics on marine ecosystem",level:"2"},{id:"sec_20_2",title:"7.2 Effect of microplastics on fresh water ecosystem",level:"2"},{id:"sec_21_2",title:"7.3 Toxic effects of microplastics shown by trophic transfer",level:"2"},{id:"sec_23",title:"8. Management of microplastics",level:"1"},{id:"sec_24",title:"9. Conclusion",level:"1"}],chapterReferences:[{id:"B1",body:'\nVerschoor A, de Poorter L, Roex E, Bellert B. Quick scan and prioritization of microplastic sources and emissions. RIVM Letter report. 2014; 5:156\n'},{id:"B2",body:'\nDuis K and Coors A. Microplastics in the aquatic and terrestrial environment: sources (with a specific focus on personal care products), fate and effects. 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Microplastics in freshwater systems: a review of the emerging threats, identification of knowledge gaps and prioritisation of research needs. Water research. 2015;75:63-82.\n'},{id:"B29",body:'\nLeslie HA. Plastic in Cosmetics: Are we polluting the environment through our personal care?: Plastic ingredients that contribute to marine microplastic litter. 2015.\n'},{id:"B30",body:'\nStrand J. Contents of polyethylene microplastic in some selected personal care products in Denmark. In International Conference on Plastics in Marine Environments. 2014.\n'},{id:"B31",body:'\nMagnusson K, Eliasson K, Fråne A, Haikonen K, Hultén J, Olshammar M, Stadmark J, Voisin A. Swedish sources and pathways for microplastics to the marine environment. A review of existing data. IVL, C. 2016;183:1-87.\n'},{id:"B32",body:'\nPoulsen PB, Stranddorf HK, Hjuler K, Rasmussen JO. Vurderingafmalingsmiljøbelastningianvendelsesfasen [Assessment of the environmental impact of paint in the use phase]. Miljøprojekt nr. Danish Environmental Protection Agency.2002;662.\n'},{id:"B33",body:'\nFabbri D, Tartari D, Trombini C. Analysis of poly (vinyl chloride) and other polymers in sediments and suspended matter of a coastal lagoon by pyrolysis-gas chromatography-mass spectrometry. Analytica Chimica Acta. 2000;413(1-2):3-11.\n'},{id:"B34",body:'\nNorén F and Naustvoll LJ. Survey of microscopic anthropogenic particles in Skagerrak. Report commissioned by Klima-ogForurensningsdirektoratet. 2010.\n'},{id:"B35",body:'\nDhodapkar S, Trottier R, Smith B. Measuring Dust and Fines In Polymer Pellets. Chemical Engineering. 2009 :1;116(9):24.\n'},{id:"B36",body:'\nOECD Series on emissions documents. Emission Scenario documents on coating industry (Paints, Lacquers and Varnishes). 2009.\n'},{id:"B37",body:'\nLeslie HA, Van Velzen MJ, Vethaak AD. Microplastic survey of the Dutch environment. Novel data set of microplastics in North Sea sediments, treated wastewater effluents and marine biota, The Netherlands. 2013 ;1-30.\n'},{id:"B38",body:'\nSiegle, L. Are loom bands the next environmental disaster?, in: The Observer. 2014.\n'},{id:"B39",body:'\nMason SA, Garneau D, Sutton R, Chu Y, Ehmann K, Barnes J, Fink P, Papazissimos D, Rogers DL. Microplastic pollution is widely detected in US municipal wastewater treatment plant effluent. Environmental Pollution. 2016 Nov 1;218:1045-54.\n'},{id:"B40",body:'\nHidalgo-Ruz V, Gutow L, Thompson RC, Thiel M. Microplastics in the marine environment: a review of the methods used for identification and quantification. Environmental science & technology. 2012 Mar 20;46(6):3060-75.\n'},{id:"B41",body:'\nMathalon A, Hill P. Microplastic fibers in the intertidal ecosystem surrounding Halifax Harbor, Nova Scotia. Marine pollution bulletin. 2014 Apr 15;81(1):69-79.\n'},{id:"B42",body:'\nVeerasingam S, Saha M, Suneel V, Vethamony P, Rodrigues AC, Bhattacharyya S, Naik BG. Characteristics, seasonal distribution and surface degradation features of microplastic pellets along the Goa coast, India. Chemosphere. 2016 Sep 1;159:496-505.\n'},{id:"B43",body:'\nDris R, Imhof HK, Löder MG, Gasperi J, Laforsch C, Tassin B. Microplastic contamination in freshwater systems: Methodological challenges, occurrence and sources. In Microplastic Contamination in Aquatic Environments 2018 Jan 1 (pp. 51-93). Elsevier.\n'},{id:"B44",body:'\nKim IS, Chae DH, Kim SK, Choi S, Woo SB. Factors influencing the spatial variation of microplastics on high-tidal coastal beaches in Korea. Archives of environmental contamination and toxicology. 2015 Oct 1;69(3):299-309.\n'},{id:"B45",body:'\nShahul Hamid F, Bhatti MS, Anuar N, Anuar N, Mohan P, Periathamby A. Worldwide distribution and abundance of microplastic: how dire is the situation?. Waste Management & Research. 2018 Oct;36(10):873-97.\n'},{id:"B46",body:'\nVan Cauwenberghe L, Devriese L, Galgani F, Robbens J, Janssen CR. Microplastics in sediments: a review of techniques, occurrence and effects. Marine environmental research. 2015 Oct 1;111:5-17.\n'},{id:"B47",body:'\nFok L, Lam TW, Li HX, Xu XR. A meta-analysis of methodologies adopted by microplastic studies in China. Science of The Total Environment. 2020 May 20;718:135371.\n'},{id:"B48",body:'\nWang J, Liu X, Li Y, Powell T, Wang X, Wang G, Zhang P. Microplastics as contaminants in the soil environment: A mini-review. Science of The Total Environment. 2019 Nov 15;691:848-57.\n'},{id:"B49",body:'\nBrach L, Deixonne P, Bernard MF, Durand E, Desjean MC, Perez E, van Sebille E, ter Halle A. Anticyclonic eddies increase accumulation of microplastic in the North Atlantic subtropical gyre. Marine pollution bulletin. 2018 Jan 1;126:191-6.\n'},{id:"B50",body:'\nLu K, Qiao R, An H, Zhang Y. Influence of microplastics on the accumulation and chronic toxic effects of cadmium in zebrafish (Danio rerio). Chemosphere. 2018 Jul 1;202:514-20.\n'},{id:"B51",body:'\nZhang Y, Gao T, Kang S, Sillanpää M. Importance of atmospheric transport for microplastics deposited in remote areas. Environmental Pollution. 2019 Nov 1;254:112953.\n'},{id:"B52",body:'\nFrias JP, Nash R. Microplastics: finding a consensus on the definition. Marine pollution bulletin. 2019 Jan 1;138:145-7.\n'},{id:"B53",body:'\nEngler RE. The complex interaction between marine debris and toxic chemicals in the ocean. Environmental science & technology. 2012 Nov 20;46(22):12302-15.\n'},{id:"B54",body:'\nAntunes J, Frias J, Sobral P. Microplastics on the Portuguese coast. Marine pollution bulletin. 2018 Jun 1; 131:294-302.\n'},{id:"B55",body:'\nFisner M, Taniguchi S, Moreira F, Bícego MC, Turra A. Polycyclic aromatic hydrocarbons (PAHs) in plastic pellets: Variability in the concentration and composition at different sediment depths in a sandy beach. Marine pollution bulletin. 2013 May 15;70(1-2):219-26.\n'},{id:"B56",body:'\nFries E, Dekiff JH, Willmeyer J, Nuelle MT, Ebert M, Remy D. Identification of polymer types and additives in marine microplastic particles using pyrolysis-GC/MS and scanning electron microscopy. Environmental Science: Processes & Impacts. 2013;15(10):1949-56.\n'},{id:"B57",body:'\nQu X, Su L, Li H, Liang M, Shi H. Assessing the relationship between the abundance and properties of microplastics in water and in mussels. Science of the total environment. 2018 Apr 15;621:679-86.\n'},{id:"B58",body:'\nLi J, Green C, Reynolds A, Shi H, Rotchell JM. Microplastics in mussels sampled from coastal waters and supermarkets in the United Kingdom. Environmental pollution. 2018 Oct 1;241:35-44.\n'},{id:"B59",body:'\nMiller ME, Kroon FJ, Motti CA. Recovering microplastics from marine samples: A review of current practices. Marine Pollution Bulletin. 2017 Oct 15;123(1-2):6-18.\n'},{id:"B60",body:'\nLima AR, Costa MF, Barletta M. Distribution patterns of microplastics within the plankton of a tropical estuary. Environmental Research. 2014 Jul 1;132:146-55.\n'},{id:"B61",body:'\nMani T, Hauk A, Walter U, Burkhardt-Holm P. Microplastics profile along the Rhine River. Scientific reports. 2015 Dec 8;5(1):1-7.\n'},{id:"B62",body:'\nPrata JC. Microplastics in wastewater: State of the knowledge on sources, fate and solutions. Marine pollution bulletin. 2018 Apr 1;129(1):262-5.\n'},{id:"B63",body:'\nGeyer R, Jambeck JR, Law KL. Production, use, and fate of all plastics ever made. Science advances. 2017 Jul 1;3(7):e1700782.\n'},{id:"B64",body:'\nIvleva NP, Wiesheu AC, Niessner R. Microplastic in aquatic ecosystems. Angewandte Chemie International Edition. 2017 Feb 6;56(7):1720-39.\n'},{id:"B65",body:'\nHartmann NB, Hüffer T, Thompson RC, Hassellöv M, Verschoor A, Daugaard AE, Rist S, Karlsson T, Brennholt N, Cole M, Herrling MP. Are we speaking the same language? Recommendations for a definition and categorization framework for plastic debris.2019\n'},{id:"B66",body:'\nRezania S, Park J, Din MF, Taib SM, Talaiekhozani A, Yadav KK, Kamyab H. Microplastics pollution in different aquatic environments and biota: A review of recent studies. Marine pollution bulletin. 2018 Aug 1;133:191-208.\n'},{id:"B67",body:'\nWright SL, Ulke J, Font A, Chan KL, Kelly FJ. Atmospheric Microplastic deposition in an urban environment and an evaluation of transport. Environment international. 2020 Mar 1;136:105411.\n'},{id:"B68",body:'\nTriebskorn R, Braunbeck T, Grummt T, Hanslik L, Huppertsberg S, Jekel M, Knepper TP, Krais S, Müller YK, Pittroff M, Ruhl AS. Relevance of nano-and microplastics for freshwater ecosystems: a critical review. TrAC Trends in Analytical Chemistry. 2019 Jan 1;110:375-92.\n'},{id:"B69",body:'\nJames E, Turner A. Mobilization of antimony from microplastics added to coastal sediment. Environmental Pollution. 2020 May 1:114696.\n'},{id:"B70",body:'\nCressey D. The plastic ocean. Nature. 2016 Aug 18;536(7616):263-5.\n'},{id:"B71",body:'\nAbidli S, Toumi H, Lahbib Y, El Menif NT. The first evaluation of microplastics in sediments from the complex lagoon-channel of Bizerte (Northern Tunisia). Water, Air, & Soil Pollution. 2017 Jul 1;228(7):262.\n'},{id:"B72",body:'\nGuilhermino L, Vieira LR, Ribeiro D, Tavares AS, Cardoso V, Alves A, Almeida JM. Uptake and effects of the antimicrobial florfenicol, microplastics and their mixtures on freshwater exotic invasive bivalve Corbicula fluminea. Science of the Total Environment. 2018 May 1;622:1131-42.\n'},{id:"B73",body:'\nZalasiewicz J, Waters CN, do Sul JA, Corcoran PL, Barnosky AD, Cearreta A, Edgeworth M, Gałuszka A, Jeandel C, Leinfelder R, McNeill JR. The geological cycle of plastics and their use as a stratigraphic indicator of the Anthropocene. Anthropocene. 2016 Mar 1;13:4-17.\n'},{id:"B74",body:'\nSilva-Cavalcanti JS, Silva JD, de França EJ, de Araújo MC, Gusmao F. Microplastics ingestion by a common tropical freshwater fishing resource. Environmental Pollution. 2017 Feb 1;221:218-26.\n'},{id:"B75",body:'\nGasperi J, Wright SL, Dris R, Collard F, Mandin C, Guerrouache M, Langlois V, Kelly FJ, Tassin B. Microplastics in air: are we breathing it in?. Current Opinion in Environmental Science & Health. 2018 Feb 1;1:1-5.\n'},{id:"B76",body:'\nRedondo-Hasselerharm PE, Gort G, Peeters ET, Koelmans AA. Nano-and microplastics affect the composition of freshwater benthic communities in the long term. Science advances. 2020 Jan 1;6(5):eaay4054.\n'},{id:"B77",body:'\nCole M, Lindeque P, Fileman E, Halsband C, Galloway TS. The impact of polystyrene microplastics on feeding, function and fecundity in the marine copepod Calanus helgolandicus. Environmental science & technology. 2015 Jan 20;49(2):1130-7.\n'},{id:"B78",body:'\nLindeque PK, Cole M, Coppock RL, Lewis CN, Miller RZ, Watts AJ, Wilson-McNeal A, Wright SL, Galloway TS. Are we underestimating microplastic abundance in the marine environment? A comparison of microplastic capture with nets of different mesh-size. Environmental Pollution. 2020 May 3:114721.\n'},{id:"B79",body:'\nMessinetti S, Mercurio S, Parolini M, Sugni M, Pennati R. Effects of polystyrene microplastics on early stages of two marine invertebrates with different feeding strategies. Environmental Pollution. 2018 Jun 1;237:1080-7.\n'},{id:"B80",body:'\nKaposi KL, Mos B, Kelaher BP, Dworjanyn SA. Ingestion of microplastic has limited impact on a marine larva. Environmental science & technology. 2014 Feb 4;48(3):1638-45.\n'},{id:"B81",body:'\nSazakli E, Leotsinidis M. Possible effects of microplastics on human health. Microplastics in Water and Wastewater, Hrissi K. Karapanagioti, Ioannis K. Kalavrouziotis Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex Close Search. 2019.\n'},{id:"B82",body:'\nSussarellu R, Suquet M, Thomas Y, Lambert C, Fabioux C, Pernet MEJ, et al. Oyster reproduction is affected by exposure to polystyrene microplastics. Proceedings of the National Academy of Sciences of the United States of America. 2016;113(9):2430-5.\n'},{id:"B83",body:'\nClark JR, Cole M, Lindeque PK, Fileman E, Blackford J, Lewis C, Lenton TM, Galloway TS. Marine microplastic debris: a targeted plan for understanding and quantifying interactions with marine life. Frontiers in Ecology and the Environment. 2016 Aug;14(6):317-24.\n'},{id:"B84",body:'\nLamb JB, Willis BL, Fiorenza EA, Couch CS, Howard R, Rader DN, True JD, Kelly LA, Ahmad A, Jompa J, Harvell CD. Plastic waste associated with disease on coral reefs. Science. 2018 Jan 26;359(6374):460-2.\n'},{id:"B85",body:'\nReichert J, Arnold AL, Hoogenboom MO, Schubert P, Wilke T. Impacts of microplastics on growth and health of hermatypic corals are species-specific. Environmental Pollution. 2019 Nov 1;254:113074.\n'},{id:"B86",body:'\nRehse S, Kloas W, Zarfl C. Short-term exposure with high concentrations of pristine microplastic particles leads to immobilisation of Daphnia magna. Chemosphere. 2016 Jun 1;153:91-9.\n'},{id:"B87",body:'\nRochman CM, Hoh E, Kurobe T, Teh SJ. Ingested plastic transfers hazardous chemicals to fish and induces hepatic stress. Scientific reports. 2013 Nov 21;3:3263.\n'},{id:"B88",body:'\nBatel A, Borchert F, Reinwald H, Erdinger L, Braunbeck T. Microplastic accumulation patterns and transfer of benzo[a]pyrene to adult zebrafish (Danio rerio) gills and zebrafish embryos. Environmental Pollution. 2018 Apr 1;235:918-30.\n'},{id:"B89",body:'\nLönnstedt OM, Eklöv P. Environmentally relevant concentrations of microplastic particles influence larval fish ecology. Science. 2016 Jun 3;352(6290):1213-6.\n'},{id:"B90",body:'\nMcGoran AR, Clark PF, Morritt D. Presence of microplastic in the digestive tracts of European flounder, Platichthys flesus, and European smelt, Osmeruseperlanus, from the River Thames. Environmental Pollution. 2017 Jan 1;220:744-51.\n'},{id:"B91",body:'\nMeng Y, Kelly FJ, Wright SL. Advances and challenges of microplastic pollution in freshwater ecosystems: A UK perspective. Environmental Pollution. 2020 Jan 1;256:113445.\n'},{id:"B92",body:'\nAu SY, Lee CM, Weinstein JE, van den Hurk P, Klaine SJ. Trophic transfer of microplastics in aquatic ecosystems: identifying critical research needs. Integrated environmental assessment and management. 2017 May 1;13(3):5059.\n'},{id:"B93",body:'\nDesforges JP, Galbraith M, Ross PS. Ingestion of microplastics by zooplankton in the Northeast Pacific Ocean. Archives of environmental contamination and toxicology. 2015 Oct 1;69(3):320-30.\n'},{id:"B94",body:'\nNelms SE, Galloway TS, Godley BJ, Jarvis DS, Lindeque PK. Investigating microplastic trophic transfer in marine top predators. Environmental Pollution. 2018 Jul 1;238:999-1007.\n'},{id:"B95",body:'\nWelden NA, Abylkhani B, Howarth LM. The effects of trophic transfer and environmental factors on microplastic uptake by plaice, Pleuronectes plastessa, and spider crab, Maja squinado. Environmental Pollution. 2018 Aug 1;239:351-8.\n'},{id:"B96",body:'\nGray AD, Weinstein JE. Size-and shape-dependent effects of microplastic particles on adult daggerblade grass shrimp (Palaemonetes pugio). Environmental toxicology and chemistry. 2017 Nov;36(11):3074-80.\n'},{id:"B97",body:'\nNolte TM, Hartmann NB, Kleijn JM, Garnæs J, Van De Meent D, Hendriks AJ, Baun A. The toxicity of plastic nanoparticles to green algae as influenced by surface modification, medium hardness and cellular adsorption. Aquatic toxicology. 2017 Feb 1;183:11-20.\n'},{id:"B98",body:'\nDong CD, Chen CW, Chen YC, Chen HH, Lee JS, Lin CH. Polystyrene microplastic particles: In vitro pulmonary toxicity assessment. Journal of hazardous materials. 2020 Mar 5;385:121575.\n'},{id:"B99",body:'\nVan Cauwenberghe L, Janssen CR. Microplastics in bivalves cultured for human consumption. Environmental pollution. 2014 Oct 1;193:65-70.\n'}],footnotes:[],contributors:[{corresp:null,contributorFullName:"Sukanya Mehra",address:null,affiliation:'
Cytogenetics Laboratory, Department of Zoology, Guru Nanak Dev University, Amritsar 143005, India
Cytogenetics Laboratory, Department of Zoology, Guru Nanak Dev University, Amritsar 143005, India
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However, 0.5–10% of patients suffer from adverse effects especially on skeletal muscle. Recently, new onset of diabetes has been reported in subjects on statin therapy. Pro- and anti-oxidant effects of statins have been reported, thus fostering a debate. Previously reported data provide evidence that statins induce alterations in intracellular calcium homeostasis and mitochondrial dysfunctions that can be counteracted by antioxidants (e.g., CoQ10, creatine, and L-carnitine). Therefore, we have proposed that statin-induced inhibition of mitochondrial respiration leads to oxidative stress that opens a calcium-dependent permeability transition pore, an event that may lead to cell death. In addition, mitochondrial oxidative stress caused by statin treatment may be a signal for cellular antioxidant system responses such as catalase upregulation, possibly explaining the alleged statins’ antioxidant properties. 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In 1993, after obtaining his Ph.D. degree (Molecular Biology) from Tokyo University, he joined Professor S. Tanuma\\'s Laboratory at Tokyo University of Science as an Assistant Professor. He obtained his second Ph.D. (Pharmaceutical Science) from Tokyo University of Science in 1999 and in 2000 was promoted to the position of Lecturer at Tokyo University of Science. Professor Uchiumi then went abroad as a post-doctoral researcher for the United States-Japan Cooperative Cancer Research Program in Professor E. Fanning’s Laboratory at Vanderbilt University, 2000-2001. Professor Uchiumi was promoted to Associate Professor and then Full Professor at Tokyo University of Science in 2010 and 2016, respectively.",institutionString:"Tokyo University of Science",institution:{name:"Tokyo University of Science",institutionURL:null,country:{name:"Japan"}}},{id:"56771",title:"Dr.",name:"Sei-Ichi",surname:"Tanuma",slug:"sei-ichi-tanuma",fullName:"Sei-Ichi Tanuma",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"95273",title:"Dr.",name:"Lori A.",surname:"Walker",slug:"lori-a.-walker",fullName:"Lori A. 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Bruns",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Colorado Denver",institutionURL:null,country:{name:"United States of America"}}},{id:"206134",title:"Prof.",name:"Grazyna",surname:"Nowak",slug:"grazyna-nowak",fullName:"Grazyna Nowak",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/206134/images/6763_n.jpg",biography:null,institutionString:null,institution:{name:"University of Arkansas for Medical Sciences",institutionURL:null,country:{name:"United States of America"}}},{id:"217239",title:"BSc.",name:"Jun",surname:"Arakawa",slug:"jun-arakawa",fullName:"Jun Arakawa",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"217242",title:"BSc.",name:"Yutaka",surname:"Takihara",slug:"yutaka-takihara",fullName:"Yutaka Takihara",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"217245",title:"BSc.",name:"Motohiro",surname:"Akui",slug:"motohiro-akui",fullName:"Motohiro Akui",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"217246",title:"BSc.",name:"Hiroshi",surname:"Hamada",slug:"hiroshi-hamada",fullName:"Hiroshi Hamada",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null}]},generic:{page:{slug:"WIS-cost",title:"What Does It Cost?",intro:"
Open Access publishing helps remove barriers and allows everyone to access valuable information, but article and book processing charges also exclude talented authors and editors who can’t afford to pay. The goal of our Women in Science program is to charge zero APCs, so none of our authors or editors have to pay for publication.
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