\r\n\tThe outcome of cancer therapy with radiation has been improving over the years due to technological progress. However, due to the biological property of cancer, current radiotherapy has limitations. Therefore, in consideration of the dynamics of tumor cells caused by radiation irradiation, attempts are being made to overcome the current drawbacks and to improve radiotherapy. It is expected that carbon ion beams, hyperthermia, oxygen effect, blood flow control, etc. will be used in the future in order to improve the treatments. This book aims to introduce research results of various radioprotective agent development research and hypoxia sensitizers.
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1. Introduction
Protozoa are unicellular eukaryotes that are able to live as parasites or as free-living organisms and interact with a great variety of environments and organisms, from bacteria to man; in addition, they represent one of most important sources of parasitic diseases. Every year, more than one million people die from complications from protozoal infections worldwide [1-5]. Of the medically relevant protozoa, Trypanosomatidae and Apicomplexa constitute a substantial group including the causative agents of several human diseases such as Chagas disease, sleeping sickness, leishmaniasis, malaria and toxoplasmosis [1,5,6]. The life cycles of these parasites are highly complex, involving different hosts and different specific interactions with a variety of cells and tissues [7- 11]. Some of these parasites live in the extracellular matrix or blood of host mammals, but the majority of them infect host cells to complete their cycle. Despite the high infection and mortality rates of these protozoa, especially in low-income populations of developing regions such as Africa, Asia and the Americas, current therapies for these parasitic diseases are very limited and unsatisfactory. The development of efficient drugs is urgently necessary, as are serious public health initiatives to improve patients’ quality of life [12-16].
The Trypanosomatidae family belongs to the order Kinetoplastida and is comprised of flagellated protists characterised by the presence of the kinetoplast, a DNA-enriched portion of the mitochondrion localised close to the flagellar pocket. The most studied pathogenic trypanosomatids are the following: (a) Trypanosoma brucei, which is responsible for sleeping sickness in Africa; (b) T. cruzi, which is the causative agent of Chagas disease in Latin America; and (c) a variety of Leishmania species that cause leishmaniasis in tropical and subtropical areas worldwide. These illnesses have been classified by the World Health Organization as neglected diseases, which affect people living in poverty in developing countries and for which no efficient therapy is available [17-19].
The Apicomplexa family encompasses a large group of protists, including approximately 5,000 known parasitic species, which are characterised by the presence of an apical complex containing a set of organelles involved in the infection process. Apicomplexan parasites infect invertebrate and vertebrate hosts, including humans and other mammals. The most serious parasitic disorder is caused by apicomplexan Plasmodium species, the etiological agent of malaria, which causes more than one million deaths annually [1]. Toxoplasmosis is another important disease caused by the apicomplexan parasite Toxoplasma gondii; it has been estimated that almost half of the human population worldwide is infected with this protozoa [20]. The life cycle of the apicomplexan parasites generally consists of complex asexual and sexual reproduction, but some differences are observable among distinct genera. Malaria transmission occurs during the blood feeding of the Anopheles mosquito, whereas toxoplasmosis is mainly transmitted by the ingestion of raw meat or contaminated cat feces.
Autophagy is a physiological self-degradative pathway essential for the maintenance of the metabolic balance in eukaryotes, leading to the turnover of cellular structures during both the normal cell cycle and during conditions of stress, such as starvation [21,22]. This process depends on double-membrane vesicles known as autophagosomes, which are responsible for the engulfment of macromolecules and organelles and the recycling of their components without an inflammatory response [23]. In eukaryotic cells, proteins known as Atgs contribute to the formation of autophagosomes and their targeting to lysosomes [24]. The autophagic machinery interfaces with many cellular pathways, such as that of the immune response and the inflammatory process, and acts as an inductor or suppressor of these processes [25]. Some molecules and organelles can undergo autophagy by specific proteins, such as in the selective pathway known as xenophagy, which is also observed in the degradation of intracellular pathogens [26,27]. The involvement of autophagy in this process has been demonstrated in the interactions of different pathogens with the host cells [28-30]. In protozoan infections, the role of autophagy has been debated in light of conflicting evidence presented in the literature, which tends to vary with the experimental model. Some studies suggest that parasites evade host cell defences using autophagy, while others suggest that the host uses autophagy to eliminate the pathogen [31-35]. However, there is no doubt that the autophagic machinery decisively influences the pathogenesis and virulence of protozoan infections; this machinery may therefore represent a promising target for drug discovery [36]. The autophagic process also occurs in the protozoa [37,38] and could occur in parallel to the host cell pathway, thus increasing the complexity of the phenomena. In the following sub-sections, the biology of Trypanosomatidae and Apicomplexa protozoa will be reviewed in relation to the role of autophagy during the infection of the host cells.
2. Trypanosomatids and autophagy
As previously mentioned, the transmission of neglected diseases caused by trypanosomatids (sleeping sickness, Chagas disease and leishmaniasis) depends on an insect vector, and the environmental change from one host to another is a drastic event for the protozoa. To complete its life cycle, many metabolic and morphological changes must occur for the parasite to survive in a new host [39-42]. In addition to the kinetoplast, other characteristic ultrastructural structures are present in these parasites, including a single mitochondrion, unique flagella, sub-pellicular microtubules, glycosomes, acidocalcisomes and reservosomes (the last one is present exclusively in T. cruzi) [8]. In the context of the remodelling of sub-cellular structures, autophagy is greatly involved in eukaryotic homeostasis (including in that of trypanosomatids). However, the deregulation of this pathway, which is induced by conditions of stress, also leads to the parasite’s death (Table 1). The sequencing of the complete genome of trypanosomatids has enabled the identification of parasitic genes [43-45]. Blast analysis comparing the trypanosome genome with yeast and mammalian genomes, with a particular emphasis on genes encoding autophagic machinery, has indicated the presence of some ATG genes in trypanosomatids [46,47]. However, the partial lack of a ubiquitin-like system, which is crucial for autophagosome formation, and the absence of cytoplasm-to-vacuole-targeting pathway orthologs suggest that these parasites have alternative autophagic features.
3. T. brucei\n\t\t\t
T. brucei is the etiological agent of sleeping sickness (or African trypanosomiasis) and is transmitted by the infected tsetse fly (Glossina sp.). After a blood feeding, procyclic trypomastigotes migrate from the insect midgut to the salivary gland where they undergo differentiation to infective metacyclic forms. Subsequently, these metacyclic trypomastigotes are inoculated into the mammalian host during the blood meal of the fly and differentiate into a proliferative bloodstream slender form. Interestingly, after a new differentiation, adapted short-stumpy forms evade the host immune system and disseminate the infection to the whole body; these forms are also able to cross the blood-brain barrier, which causes severe behavioural abnormalities, such as somnolence during daytime [48] (Figure 1). Unlike all other pathogenic trypanosomatids, which have an intracellular life-stage, T. brucei remains in the bloodstream of the mammalian host throughout the process of infection and, as such, is exposed to different environmental conditions that can trigger autophagy.
3.1. Role of autophagy in T. brucei\n\t\t\t\t
The first report on this parasite and autophagy was published in the 1970s by Vickerman and colleagues. These authors described the presence of myelin-like structures in different forms of the parasite observed by transmission electron microscopy [49, 50]. Many years later, it was suggested that the autophagic pathway is involved in the turnover of glycosomes during protozoan differentiation [51]. Glycosomes are peroxysome-like organelles that perform early glycolytic steps and are also involved in lipid metabolism. It was demonstrated that glycosome contents are altered depending on the form of the parasite, with many of these organelles being close to glysosomes during the differentiation process. A similar phenomenon was observed after nutrient deprivation of the parasite, reinforcing the fact that differentiation may cause the degradation of glycosomes by pexophagy.
Further genomic and bioinformatic analyses were performed that identified in T. brucei many ATG orthologs to those of yeasts and mammals [47,52]. These genes are involved in different steps of the autophagic pathway, such as induction (ATG24, PEX14, TOR1 and TOR2, VAC8), vesicle nucleation (ATG6, VPS15 and VPS34) and vesicle expansion and completion (ATG3, ATG7, ATG9, two isoforms of ATG4 and ATG8). Two isoforms of Atg4 and two of Atg8 were recently characterised structurally [53], and it was postulated that Atg8.2 is essential for autophagosome formation and that Atg8 depletion is associated with delayed cell death [54].
It is thought that many drugs may trigger autophagy in African trypanosomes. Dihydroxyacetone (DHA), spermine (snake venom) and vasoactive intestinal peptide (VIP – a neuropeptide secreted by the immune system) induce the appearance of morphological features of autophagy in T. brucei [55-58]. DHA is an interesting compound to be used in therapy for sleeping sickness because its phosphorylation is DHA kinase-dependent, and DHA kinase is present in mammals and other eukaryotes but not in trypanosomes. After DHA uptake, this compound is not eliminated, leading to typical morphological characteristics of autophagy similar to those found in rapamycin treatment. In another report [59], the authors showed that hydrogen peroxide can produce the appearance of autophagic profiles, suggesting that the release of reactive oxygen species acts as a signal in the autophagic pathway in T. brucei, as it does in other eukaryotic cells [60-62].
Figure 1.
T. brucei life cycle.
4. T. cruzi
T. cruzi is the causative agent of Chagas disease. It is mainly transmitted by triatomine bugs, which are commonly known as “kissing bugs”. In the insect midgut, proliferative forms of the parasite called epimastigotes differentiate to metacyclic trypomastigotes after migration to the posterior intestine. During the blood meal, triatomines eliminate urine and feces with infective trypomastigotes that then gain access to the vertebrate bloodstream. After internalisation in the host cell, trypomastigotes remain in parasitophorous vacuoles (PV) that fuse with lysosomes, allowing an acidification of this compartment, which is an essential step towards differentiation into proliferative amastigotes. In the cytosol, successive parasite cycles occur until a new intracellular differentiation to trypomastigotes occurs; it is these forms that are responsible for the infection and dissemination to other cells and tissues [8] (Figure 2).
Figure 2.
T. cruzi life cycle.
4.1. Role of autophagy in T. cruzi\n\t\t\t\t
Ultrastructural evidence of autophagy in T. cruzi was observed after the treatment of epimastigotes and bloodstream trypomastigotes with drugs; the appearance of myelin-like figures was the most recurrent feature detected [63-67]. Recently, the synergistic combination of amiodarone and posoconazole was able to trigger autophagy in replicative amastigotes [68]. In this way, different classes of therapeutic agents are able to induce the formation of autophagosomes, an event associated with parasite-related autophagic cell death, being the interplay between other programmed cell death as apoptosis or necrosis not discarded [69]. Due to the limitations of cell models, previous studies of different parasite forms have employed alternative techniques, such as monodansylcadaverine (MDC) staining and ATG gene expression, to demonstrate autophagy in the parasite [66,67]. Unfortunately, T. cruzi molecular machinery does not allow the use of double-stranded RNA to knock down target RNAs [70]; in addition, the lack of recognition of protozoan proteins by anti-Atg commercial antibodies hampers the evaluation of autophagy in this parasite. In spite of the advances in molecular and cellular biology, transmission electron microscopy remains a gold standard for autophagy analysis [71,72].
Aside from the description of autophagosomes in all T. cruzi life stages, description of the Atg cascade involved in autophagosome formation is not complete. Almost all T. brucei ATG genes have ortholog genes in T. cruzi [37,47]. In this parasite, two isoforms of Atg8 were described, with only Atg8.1 localised in autophagosomes as expected. These data suggest that there is only partially shared autophagic machinery, as is observed in human Atg8 orthologs [37]. In another study [37], the authors described the participation of T. cruzi Atg4 and Atg8 isoforms under conditions of nutritional stress and in the differentiation process from epimastigotes to metacyclic trypomastigotes, a process known as metacyclogenesis. The authors observed a remarkable expression of Atg8.1 by immunofluorescence microscopy, which was suggestive of intense autophagy in differentiating epimastigotes. Moreover, Atg8 co-localised with reservosomes, which are pre-lysosomal compartments related to energy supply that are present only in epimastigotes [73,74]. The reservosomal content consumed during metacyclogenesis and the presence of Atg8 in this organelle strongly suggest that there is crosstalk between autophagy and reservosomes [75,76]. Transmission electron microscopy studies have produced images from endoplasmic reticulum profiles surrounding reservosomes that indicate the possible origin of preautophagosomal structures [66]. It is well known that PI3K inhibitors, such as 3-methyladenine and wortmannin, prevent autophagy in different experimental models [54,66]; however, these data are controversial due to a previous report demonstrating that treatment with kinase inhibitors staurosporine, genistein, 3-methyladenine and wortmannin led to the formation of autophagosomes [77]. The data indicate the necessity of careful use of PI3K inhibitors to block autophagy and the urgent need for the development of new specific autophagic inhibitors [78].
4.2. Host cell autophagy and T. cruzi infection
Though thought to be essential for parasite success, lysosomal fusion could be involved in autophagy during host cell interaction and might contribute to the process of degradation and elimination of T. cruzi. In 2009, the role of autophagy in parasite entry and co-localisation with the PV was described, resulting in increased infection of Chinese hamster ovary cells; this observation was subsequently confirmed in macrophage and heart cell lineages [34,79]. Starvation conditions and the addition of rapamycin led to an increase in the scale of the infection; this increase was partially reversed by 3-methyladenine, wortmannin and vinblastine, suggesting that autophagy favours the parasite during T. cruzi-host cell interactions. However, other groups demonstrated that classical autophagic stimuli (nutritional stress and rapamycin) did not produce an increase in parasite proliferation or even in the number of infected cells [33]. Recently, studies have emphasised role of autophagy in the control of T. cruzi infection using different cells and parasite strains (Figure 3) [80,81]. Once more, the conflicting data presented in the literature need to be further debated in light of the complexity of the protozoal strains and host cell models employed.
5. Leishmania species
The other medically important trypanosomatids are Leishmania species. Leishmaniasis is transmitted to mammals by sandflies, mainly of the Phlebotomus and Lutzomia genuses. Amastigotes differentiate into replicative procyclic promastigotes in the digestive tract of these sandflies, proliferate in the Phlebotominae gut, and then migrate to the proboscis where a new differentiation occurs to metacyclic promastigotes, the infective forms of the parasite. During the sandflies’ blood meals, metacyclic promastigotes are inoculated into mammalian tissue and are phagocytised by macrophages. Inside the host cells, promastigotes differentiate into amastigotes that replicate and are responsible for cell lysis and dissemination in the organism (Figure 4). Currently, more than 20 species of Leishmania are known, each causing different clinical manifestations of the disease, including cutaneous leishmaniasis and visceral leishmaniasis (or Kala-azar). The pathogenicity depends on the Leishmania species and the host’s immune response [8].
Figure 3.
Autophagy in T.cruzi–host cell interaction. Romano et al [34] showed the co-localization of parasite vacuole with Atg proteins in the beginning of infection (1). Moreover, the replication of amastigotes is the same with or without autophagy induction (2) [33,34]. Rapamycin and starvation control infection reducing the number of amastigotes per cell (3) [80,81].
Figure 4.
Leishmania sp. life cycle.
5.1. Role of autophagy in Leishmania sp.
Many groups have investigated autophagy cell death induced by drugs or antimicrobial peptides in various Leishmania species using electron microscopy and MDC staining [82-89]. Bioinformatics analysis has been a crucial checkpoint in the characterisation of ATG and TOR pathways in trypanosomatids [38,47,90]. In 2006, the role of autophagy in the differentiation process of L. major and L. mexicana was first evaluated [38,90]. The authors developed L. major VPS4, a mutant that could not complete the differentiation to the infective forms due to interference in autophagosome formation during conditions of starvation. The increase in Atg8 expression in differentiating forms supports the hypothesis that autophagy plays a pivotal role in metacyclogenesis [38,91]. In L. mexicana, the lack of cysteine peptidases CPA and CPB impairs autophagosomes formation and parasite differentiation; this finding is corroborated by the results of wortmaninn treatment and ATG deletion [90].
Recently, a subunit of protein kinase A in L. donovani that interferes with autophagy and protozoa differentiation was identified [92]. As observed in other trypanosomatids, the presence of Atg8-like proteins and their association with Atg4 in Leishmania species indicates that these proteins play a role in vesicle expansion [93]. Interestingly, the Atg5-Atg12 complex involved in autophagosome elongation was not previously detected [47], but recent studies have demonstrated its existence. It has also been shown that Atg5 deletion severally affects parasite homeostasis, producing a phenotype characterised by mitochondrial disruption, phospolipid accumulation and abnormal promastigote morphology [93,94]. Table 1 summarises the autophagic events in the three pathogenic trypanosomatids described in this chapter.
Summary of autophagic events in trypanosomatids. DHA: Dihydroxyacetone; DTT: dithiothretiol; SBIs: sterol biosynthesis inhibitors; LPAs: lysophospholipid analogues; MBHA: Morita–Baylis–Hillman adduct.
5.2. Host cell autophagy and L. amazonensis infection
The connection between the endosomal/lysosomal pathway and the PV results in macromolecules being taken up by the parasite, as demonstrated in T. cruzi infection [96]. In this context, a notable increase in the proliferation of L. amazonensis amastigotes was observed after autophagic induction by nutritional deprivation, rapamycin treatment or interferon-gamma. This mechanism was partially reversed by the autophagic inhibitors wortmaninn or 3-methyladenine, which significantly reduced amastigote replication (Figure 5) [33]. However, a recent report presented no correlation between the increase in LC3 expression and heightened L. amazonensis infection after treatment with autophagy inducers and inhibitors. In addition, macrophage autophagy was observed in inflammatory infiltrates of L. amazonensis-infected mice [97] and in natural human L. donovani infection [98].
Figure 5.
Autophagy in L. amazonensis-host cell interaction. When autophagy is induced, more amastigotes replicate and PV is smaller than in basal autophagic cells. Also, more lipid bodies are present, increasing infection and signaling to replication [33,97].
6. Apicomplexa and autophagy
The phylum Apicomplexa comprises one of the most medically relevant groups of protists, which cause serious health and economic problems. Among these parasites, Toxoplasma\n\t\t\t\tgondii and Plasmodium species are well-known apicomplexans; it is estimated that malaria caused by P. falciparum kills over a million people annually. Another widespread disease is toxoplasmosis, which is caused by the apicomplexan parasite T. gondii; the severity of disease caused by this organism is directly related to patients´ immunosuppression and is characterised by congenital transmission. In this context, knowledge of the detailed mechanisms involved in parasite infection and survival, including the role of autophagy, could contribute important information to the development of novel strategies for controlling Apicomplexa infections. Autophagy is an evolutionarily conserved pathway found in all eukaryotes, from unicellular organisms to metazoans; orthologs for approximately 30% of autophagy-related genes have been detected in apicomplexan sequenced genomes [99].
Among the key molecules involved in early autophagy steps, Atg1/ULK complex, Atg8 and Atg9 play crucial roles in cargo selectivity and in autophagosome formation [100,101]. Unlike other cell models, in Apicomplexa protozoa, the Atg8 C-terminal appears to not undergo processing before its association with phosphatidylethanolamine (PE) in the membrane of autophagosomes, suggesting a different regulation of this Atg protein in these organisms than in mammals and fungi [102]. Using a technique to detect lipidated Atg8 in Plasmodium species, only a single band corresponding to ATG8 was observed, suggesting that this parasite’s Atg8 exists predominantly in the PE-conjugated form [22].
Two important kinases have opposing roles in the autophagic process: TOR (target of rapamycin) and class III phosphatidylinositol3-kinase (PI3K) [78,103]. In well-established autophagic models, TOR and class III PI3K represent negative and positive regulators, respectively, that act through complexes with regulatory subunits orchestrated by signalling cascades. Analysis of the T. gondii genome revealed the presence of TOR and PI3K but not of other proteins crucial to the formation of these complexes [99]. Curiously, no genes for TOR complex machinery were found in the Plasmodium genome. Thus, it is possible that these unicellular eukaryotes have specific unknown proteins for several steps of the autophagic pathway instead of an absence of key proteins [22,104].
7. T. gondii\n\t\t\t
T. gondii is an obligate intracellular parasite with a complex life cycle involving one definitive feline host where the sexual phase occurs and intermediate hosts, such as birds, other mammals and man [105]. The main transmission routes to humans are the following: (i) the ingestion of raw meat containing tissue cysts (essentially bradyzoites forms); (ii) the ingestion of water and food contaminated with feline feces residue containing oocysts; and (iii) transplacentary pathway of tachyzoites [106]. After oral ingestion, tissue cysts or oocysts rupture, liberating the slow-replicating forms known as bradyzoites and sporozoites, respectively, which then invade intestinal epithelial cells. In the intracellular environment, the parasites differentiate into the fast-replicating tachyzoites that proliferate inside the host cell PV. The sustained infection depends on the modification of the PV membrane by the insertion of T. gondii secreted proteins, which prevent the fusion to lysosomes and, consequently, the elimination of the parasite (Figure 6) [20,107].
In healthy adults, T. gondii cysts are established in the host cells mainly in the eyes, brain and muscles during the chronic phase of toxoplasmosis [108]; however, in immunocompromised patients, such as HIV-positive patients, or in congenital toxoplasmosis, the disease becomes much more severe, and its complications could lead to death [20,109,110]. Despite the high percentage of people infected, the available therapy for toxoplasmosis is effective only in the tachyzoite stage and presents limited efficacy against the tissue cyst, which is the latent form of the parasite [111]. In this context, many efforts are necessary to develop new drugs to treat T. gondii infection [17].
7.1. Role of autophagy in T. gondii infection
Only a few studies on the T. gondii autophagic pathway have been performed, and these studies suggest opposing roles of autophagy in the parasite infection [102,112]. The presence of TgAtg8 in autophagic vesicles was observed in tachyzoites during their intracellular replication; similarly, severe parasite growth arrest due to TgAtg3 knockdown and recent identifications of the presence of TgAtg1 and TgAtg4 in the parasite suggest a role for autophagy in T. gondii homeostasis, although long-term exposure to autophagic stimuli was found to be harmful to the parasite (Figure 7) [112; 113].
Tachyzoites divide by a process called endodyogeny, whereby two daughter cells are developed inside a mother cell and leave residual material at the end of division. During this process, autophagy might be involved in recycling the mother cell organelles, such as micronemes and rhoptries, which are synthesised de novo in the daughter cells; however the accumulation of organelles after endodyogeny has not been observed in TgATG3 knockout organisms, making other experiments necessary to confirm this hypothesis [113]. One important phenotype detected in autophagic mutants is the loss of mitochondrial integrity [102,112]. Mitophagy, which is the autophagy of mitochondria, regulates the mitochondrial number to match metabolic demand; this process represents a quality control that is necessary for the removal of damaged organelles [114]. Autophagic stimuli are able to direct the mitochondrial network of tachyzoites towards their autophagic pathway, but the molecular machinery involved in selective targeting of the organelle remains unclear [102,112]. Nutrient deprivation has been shown to be a classic stimulus for the autophagic pathway activation in a large variety of organisms [37,115]. In T. gondii tachyzoites, starvation induces autophagy in extracellular and intracellular parasites [102,112]. Furthermore, autophagosomes were observed in parasites after a long extracellular nutritional restriction, suggesting that autophagy can act as a mechanism of resistance to starvation for nutrient recycling until the infection of a new host cell [102].
Figure 6.
T. gondii life cycle. (1) Definitive host infection; (2) Cyst disruption and intestinal epithelial cell infection; (3) Formation of merozoites; (4,5) Start of sexual phase with the formation of macrogametes and flagellate microgametes from merozoites; (6) Fusion of microgamete and macrogamete; (7) Oocyst release to the environment in the faeces; (8) The unsporulated oocysts become infective and contaminate the environment [116-118]; (9) The sporulated oocysts can cause infection of animals via consumption of contaminated food and water. (10,11) Human infection occurs by the ingestion of raw or undercooked meat of infected animals containing T. gondii cysts; (12) T. gondii tachyzoite multiplication in the intermediate host; (13) Tachyzoite-bradyzoite differentiation and formation of tissue cysts; (14) Transplacentary transmission of tachyzoites.
Figure 7.
T. gondii tachyzoites response to autophagic stress. Autophagy acts in survival or death mechanisms in apicomplexan parasites depending on the environmental stress conditions. Arrows: activation; Headless arrows: inhibition.
The data presented here demonstrate possible functions of T. gondii autophagy in parasite homeostasis. However, it has been proposed that, when strongly induced, the autophagic pathway represents a self-destructive mechanism leading to protozoal death. The molecular pathway of autophagic cell death is still unknown, and it is debated whether the pathway is a type of programmed cell death or a survival response to death stimuli [119]. Intracellular starved tachyzoites showed systematic mitochondrial fragmentation and a defect in host cell internalisation. As T. gondii is an obligate intracellular protozoa, the loss of invasion capacity leads to parasite death. The impairment in infective ability was related to the loss of mitochondrial integrity because organelles from apical complexes, such as rhoptries and micronemes, which are usually associated with the invasion process, are intact in these parasites [112]. Interestingly, these authors also demonstrated that autophagic inhibitor 3-methyladenine prevented mitochondrial fragmentation, suggesting autophagic involvement in T. gondii death.
While nutritional stress has been extensively used as a model for autophagy, this condition is not easily encountered in the host cells and tissues in vivo. However, parasites could be exposed to nutritional restriction in the extracellular environment. The viability of tachyzoites kept in an axenic medium for periods of up to 12 hours drastically decreases, but a significant number of parasites nevertheless differentiate into bradyzoites [120]. Indeed, these observations raise the hypothesis that autophagy could be an adaptive mechanism of T. gondii to survive for short periods in starvation conditions, allowing the parasite to recover when favourable conditions occur or even to differentiate into a cystic form. Another interesting point for discussion is the correlation between mitochondrial fragmentation in intracellular tachyzoites and the depletion of amino acids in the culture medium [112]. Activated macrophages infected with the parasite showed low availability of the essential amino acid tryptophan, a condition that directly contributes to the protozoa’s death in these cells [121,122]. In this context, TOR kinase is a vital component of the amino acid sensing mechanism in eukaryotic cells, as suggested by the detection of TgTOR by bioinformatic approaches and the evaluation of the activity of the classical TOR inhibitor rapamycin. This inhibitor triggered mitochondrial fragmentation of intracellular tachyzoites in starved parasites, and this phenotype was reversed by adding 3-methyladenine [112].
7.2. Host cell autophagy and T. gondii infection
As previously mentioned, T. gondii can infect any nucleated cell, but the parasite tropism principally involves nervous and muscular cells where the establishment of cystic forms is observed in chronic toxoplasmosis [111,123]. As was observed for T. cruzi-host cell interactions, controversial data on the importance of autophagy during T. gondii infection have been described in the literature; indeed, it has been suggested that autophagy can either control or facilitate parasite internalisation and proliferation [32,35,124-128]. Despite the relevance of muscular and nervous cells for the establishment of infection and for the course of the disease, very little has been reported on the role of autophagy in the progression of infection. As we will discuss in the next paragraphs, previous studies on the connection between the autophagic pathway and T. gondii infection were performed in macrophages, which are cells that play an important role in the immune response against this parasite [129].
Previous reports have shown that cellular immunity mediated by CD40 stimulation redirects the T. gondii to a lysosomal compartment via the autophagic route, resulting in the antimicrobial activity of the macrophage in vitro and in vivo [124,125]. In vivo, parasite elimination was dependent on GTPase p-47, IFN-γ, IGTP, and PI3K and culminated in the rupture of the parasite’s membrane [125] (Figure 8). Additionally, the relationship between autophagy and the fusion of lysosomes with the T. gondii PV seems to be dependent on the synergy between TRAF6 signalling downstream of CD40 and TNF-α [126]. However, the IFN-γ/p47 GTPase-dependent elimination of the parasite by macrophages is independent of CD40/TNF signalling in vitro, demonstrating the primary role of IFN-γ in immunity against T. gondii in mice [127]. As observed in astrocytes, autophagy is activated to eliminate intracellular parasite debris and thus prevent the host cell death. Investigations in macrophages also indicated that the CD40-p21-Beclin 1 pathway is a CD40-dependent immunity route to mediating in vivo protection [128]. Similarly, Atg5 is required for damage to the PV membrane and removal of the parasite in primary macrophages stimulated by IFN-γ, despite the fact that no autophagosomes involving T. gondii have been detected. Atg5 also appeared crucial for in vivo p47 GTPase IIGP1 recruitment to the vacuole membrane induced by IFN-γ, suggesting an additional autophagy-independent role for Atg5 in the GTPase trafficking process [32]. In T. gondii infected astrocytes, the participation of autophagy has been shown to be indirect. The IFN-γ-stimulation of astrocytes infected with tachyzoites triggers the recruitment of p47 GTPases to the PV and usually leads to rupture of the vacuole and parasite membrane. In this case, autophagy acts by removing protozoal debris that accumulates in the cytoplasm and causes cell injury. Additionally, autophagy assists in antigen presentation through MHC class II in astrocytes, allowing an intracerebral immune response to parasite [130].
So far, little has been described regarding the involvement of autophagy in the interaction of T. gondii with nonprofessional phagocytes. In primary fibroblasts or Hela cells, infection with tachyzoites induced LC3 conjugation to PE, accumulation of LC3-containing vesicles close to the PV and an overexpression of beclin-1 and phosphatidylinositol-3-phosphate in the host cells in the mTOR-independent pathway. The infection of Atg5-deficient fibroblasts was reduced in physiological concentrations of amino acids, reinforcing the host cell autophagic role in the recovery of nutrients by the parasite. Because the classical function of autophagy involves recycling of various cellular components and because T. gondii depends on the uptake of many nutrients from the host cell, it has been proposed that the parasite may take advantage of the mammalian autophagic machinery to achieve successful infection [35]. Table 2 shows the host autophagic roles during T. gondii infection.
Figure 8.
Autophagic role in T. gondii interaction with professional phagocytic cells. (a) INF-Y recruits P47GTPases to the PV membrane and induce nitric oxide production which limits the parasite replication. (b) CD40L activates Atg5 and recruits the autophagic machinery to the PV membrane. (c) PV and parasite membrane degradation by P47GTPase and Atg5. (d) Elimination of T. gondii debris by autophagolysosomal fusion and possible contribution of this process in antigen presentation through class II MHC.
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t\t
\n\t\t\t\tHost cell\n\t\t\t
\n\t\t\t
\n\t\t\t\tInduction\n\t\t\t
\n\t\t\t
\n\t\t\t\tPhenotype\n\t\t\t
\n\t\t\t
\n\t\t\t\tReference\n\t\t\t
\n\t\t
\n\t\t
\n\t\t\t
Peritoneal Macrophages and RAW264.7 lineage
\n\t\t\t
CD40 stimulation and rapamycin
\n\t\t\t
accumulation of LC3 around PV and low parasite load
Plasmodium species are causative agents of malaria, the illness with the highest morbidity rate among human parasitic diseases. Currently, 5 species of Plasmodium sp. (P. falciparum, P. vivax, P. malariae,\n\t\t\t\tP. ovale and P. knowlesi) can infect humans, and lethality is associated with P. falciparum [131-133]. Sporozoites are transmitted by Anopheles sp. mosquitoes (definitive hosts) to the mammals (intermediate hosts), where they migrate primarily to the liver. After internalisation in hepatocytes, the parasites convert from elongated sporozoites (invasion competent and motile) to round proliferative trophozoites (metabolically active), which start the asexual reproduction process known as schizogony. At the end of the reproductive process, the daughter cells (merozoites) initiate maturation for erythrocyte invasion. When the merozoites become mature, they are enclosed in a membrane (the merosome) and released from hepatocytes to invade red blood cells, causing clinical symptoms of malaria (Figure 9). [135-137].
Figure 9.
Plasmodium sp. life cycle. (1) Inoculation of sporozoites by malaria-infected female Anopheles mosquito into the human host. (2) Sporozoites infect hepatocytes. (3) Sporozoite-trophozoite differentiation. (4) Schizont formation. (5) Schizont rupture and release of merozoites. (6) Merozoites infect red blood cells. (7,8) Trophozoite maturation. (9) Schizont formation in red blood cells. (10) Schizont rupture and release of merozoites. (11) Infection of new red blood cells by the merozoites. (12,13) Differentiation of some parasites in gametocytes (sexual erythrocytic stages). (14) Ingestion of gametocytes by the mosquito during a blood meal. (15) Zygote formation in the mosquito´s stomach when the microgametes penetrate the macrogametes. (16) Zygote-ookinete differentiation. (17) Ookinetes invade the midgut wall of the mosquito where they develop into oocysts. (18,19) Oocysts rupture and release sporozoites. (20) Sporozoites migrate to the mosquito\'s salivary glands. (21) Mosquito inoculates sporozoites into a new human, perpetuating the parasite cycle.
8.1. Role of autophagy in Plasmodium sp. infection
Recent publications have suggested that autophagy is involved in the differentiation of sporozoites to merosomes in hepatocytes [137,138]. The sporozoite-to-trophozoite differentiation is accompanied by the elimination of organelles unnecessary for schizogony and the production of merozoites in liver cells [137]. For example, micronemes and rhoptries are compartmentalised in the cytoplasm of sporozoites and sequestered in double-membrane structures resembling autophagosomes. In axenic conditions, the treatment of parasites with 3-methyladenine resulted in significant delay of the sporozoite differentiation process [139]. After sporozoite differentiation, Atg8 is present in autophagosomes during the replication phase, suggesting an additional independent role for this protein in autophagy [137, 138,140].
The involvement of autophagy in Plasmodium-infected red blood cells has been poorly studied. One study demonstrated that erythrocytes infected with P. falciparum trophozoites and maintained in supplemented culture medium expressed Atg8 in the parasite cytosol. However, when these infected cells are submitted to restriction of glucose and amino acids, an increase in the number of autophagosomes labelled by Atg8 was observed, and these vesicles were found close to red blood cell membranes. Once erythrocytes no longer have organelles in the cytoplasm, the potential targets of autophagosomes in this cell model are debated. One hypothesis suggested that these autophagosomes target haemoglobin and blood nutrients to favour nutrient uptake by the parasite (Gaviria and colleagues, unpublished results). Surprisingly, no TOR ortholog was found in the P. falciparum genome (Sinai & Roepe, unpublished results), suggesting that under normal growth conditions, P. falciparum autophagy is configured as a survival process that is constitutively regulated by the acquisition of nutrients, although this route is unusual. Table 3 summarises the published reports on autophagic features in apicomplexans.
Little is known about the involvement of autophagy in the Plasmodium sp.-host cell interactions. So far, Plasmodium ATG8 knock-out resulted in a lethal phenotype, indicating that this gene is essential for the mammalian life-stage of the parasite [22]. However, there have been no studies on the importance of the host cell autophagic machinery during the infection.
The present chapter addresses the positive and negative regulations of the autophagic process of infected mammalian cells and the possible effects of these regulations on the in vitro and in\n\t\t\t\tvivo modulation of this process. This review also describes the autophagy pathway in pathogenic trypanosomatids and apicomplexans responsible for some of the most relevant neglected illnesses worldwide. The pivotal role of autophagy in pathogenicity and virulence was demonstrated in T. cruzi, T. brucei, Leishmania sp., T. gondii and Plasmodium sp., which suggests that autophagic machinery is a possible target for anti-parasitic intervention.
Acknowledgments
This work was supported with grants from CNPq (Universal), FAPERJ (APQ1) and IOC/FIOCRUZ.
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S.",surname:"Menna-Barreto",fullName:"Rubem Menna-Barreto",slug:"rubem-menna-barreto",email:"rubemb@ioc.fiocruz.br",position:null,institution:null},{id:"167537",title:"M.Sc.",name:"Thabata",middleName:null,surname:"Duque",fullName:"Thabata Duque",slug:"thabata-duque",email:"thaduque@uol.com.br",position:null,institution:null},{id:"167538",title:"Mrs.",name:"Xênia",middleName:null,surname:"Souto",fullName:"Xênia Souto",slug:"xenia-souto",email:"xeniapop@hotmail.com",position:null,institution:null},{id:"167539",title:"MSc.",name:"Valter",middleName:null,surname:"Andrade-Neto",fullName:"Valter Andrade-Neto",slug:"valter-andrade-neto",email:"valter@ioc.fiocruz.br",position:null,institution:null},{id:"167540",title:"MSc.",name:"Vitor",middleName:null,surname:"Ennes-Vidal",fullName:"Vitor Ennes-Vidal",slug:"vitor-ennes-vidal",email:"vitorennesvidal@gmail.com",position:null,institution:null}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Trypanosomatids and autophagy",level:"1"},{id:"sec_3",title:"3. T. brucei\n\t\t\t",level:"1"},{id:"sec_3_2",title:"3.1. Role of autophagy in T. brucei\n\t\t\t\t",level:"2"},{id:"sec_5",title:"4. T. cruzi",level:"1"},{id:"sec_5_2",title:"4.1. Role of autophagy in T. cruzi\n\t\t\t\t",level:"2"},{id:"sec_6_2",title:"4.2. Host cell autophagy and T. cruzi infection",level:"2"},{id:"sec_8",title:"5. Leishmania species",level:"1"},{id:"sec_8_2",title:"5.1. Role of autophagy in Leishmania sp.",level:"2"},{id:"sec_9_2",title:"5.2. Host cell autophagy and L. amazonensis infection",level:"2"},{id:"sec_11",title:"6. Apicomplexa and autophagy",level:"1"},{id:"sec_12",title:"7. T. gondii\n\t\t\t",level:"1"},{id:"sec_12_2",title:"7.1. Role of autophagy in T. gondii infection",level:"2"},{id:"sec_13_2",title:"7.2. Host cell autophagy and T. gondii infection",level:"2"},{id:"sec_15",title:"8. Plasmodium sp.",level:"1"},{id:"sec_15_2",title:"8.1. Role of autophagy in Plasmodium sp. infection",level:"2"},{id:"sec_17",title:"9. Conclusion ",level:"1"},{id:"sec_18",title:"Acknowledgments",level:"1"},{id:"sec_18",title:"Acknowledgments",level:"2"}],chapterReferences:[{id:"B1",body:'Nayyar GML, Breman JG, Newton PN, Herrington J. Poor-quality antimalarial drugs in southeast Asia and sub-Saharan Africa. Lancet Infectious Diseases 2012;12(6):488-96.'},{id:"B2",body:'Soeiro MN, De Castro SL. Trypanosoma cruzi targets for new chemotherapeutic approaches. Expert Opinion on Therapeutic Targets 2009;13(1):105-21.'},{id:"B3",body:'Kobets T, Grekov I, Lipoldova M. Leishmaniasis: prevention, parasite detection and treatment. Current Medicinal Chemistry 2012;19(10): 1443-74.'},{id:"B4",body:'Welburn SC, Maudlin I. Priorities for the elimination of sleeping sickness. Advances in Parasitology 2012;79:299-337. '},{id:"B5",body:'Centers for Disease Control and Prevention. 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Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, RJ, Brazil
Laboratory of Cell Biology, Department of Biology, Federal University of Juiz de Fora, MG, Brazil
Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, RJ, Brazil
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\n
1. Introduction
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Wear is the damaging, gradual removal or deformation of material at solid surfaces. Causes of wear can be mechanical also called as erosion or chemical also called as corrosion. Wear of metals occurs by plastic displacement of surface and near-surface material and by detachment of particles that form wear debris. In material science, wear is the erosion of material from a solid surface by the action of another solid. The study of the process of wear is the part of the theory of tribology. Wear in machine components, along with different cycles, for example, fatigue and creep, makes surfaces deteriorate, in the end prompting material degradation or loss of applicability. Subsequently, wear has enormous monetary significance as first mentioned in the Jost Report. Abrasive wear alone has been assessed to cost 1–4% of the gross national product of industrialized countries. Wear of metals happens by plastic dislodging of surface and close to surface material and by separation of particles that produce wear debris. The molecule size may change from millimeters to nanometers. This cycle may happen by contact with different metals, nonmetallic solids, streaming fluids, solid particles or fluid beads entrained in streaming gasses. The wear rate is influenced by components, for example, sort of stacking (e.g., stationary and active), kind of movement (e.g., gliding and continuing), surrounding temperature, and lubrication, specifically by the cycle of deposition and deterioration of the boundary lubrication layer. Contingent upon the tribosystem, diverse wear types and wear systems can be watched.
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2. Industrial wear problems
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The Table 1 represents the various wear problems occur in the industries.
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Sl no.
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Industrial wear problems
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Significant characteristic
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Examples
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1.
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The wear of surfaces by hard particles in a stream of fluid
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Erosion with one supply of erodent being continuously renewed in a gas or fluid
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Valves controlling flow of crude oil laden with sand Gas pumping equipment
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2.
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The wear of surfaces by hard particles in a compliant bed of material
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Abrasion, with supply of abrasive continuously renewed by movement of bed of material
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Digger teeth. Rotors of powder mixes. Extrusion dies for bricks and tiles
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3
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Wear of metal surfaces in mutual rubbing contact, with abrasive particles present
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Three body abrasion (solid abrasive-solid) with an ongoing supply of new abrasive particles
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Pivot pins in construction machinery. Scraper blades in plaster mixing machines. Shaft seals for fluids containing abrasives
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4.
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The wear of metal components in rubbing contact with a sequence of other solid components
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Adhesive wear and abrasion, but with one component in the wear process being continuously renewed
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Tools used in manufacture, such as punching and pressing tools, sintering dies and cutter blades
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5.
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The wear of pairs of metal components in mutual and repeated rubbing contact
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Adhesive wear, but with a wear rate that can be very variable depending on the detailed operating conditions
\n
Piston rings and cylinder liners. Coupling teeth and splines. Fretting between machine components
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6.
\n
Component wear from rubbing contact between metals and non metals
\n
Adhesive wear between two consistent components
\n
Brakes and clutches. Dry rubbing bearings. Artificial hip joints
\n
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Table 1.
Examples of industrial wear problems.
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3. Types of wear
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3.1 Abrasive Wear
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Removal of material by the mechanical action of an abrasive is known as abrasive wear (Figure 1). Abrasives are substances which are usually harder than the abraded surface and have an angular profile. Examples: sand particles between contact surfaces, the damage of crankshaft journals in reciprocating compressors. Abrasive wear is ordinarily ordered by the kind of contact and the contact condition. The sort of contact decides the method of abrasive wear. The two methods of abrasive wear are known as two-body and three-body abrasive wear. Two-body wear happens when the sand or hard particles eliminate material from the contrary surface. The basic similarity is that of material being eliminated or dislodged by a cutting or plowing activity. Three-body wear happens when the particles are not constrained, and are allowed to roll and slide down a surface. The contact condition decides if the wear is delegated open or shut. An open contact condition happens when the surfaces are adequately uprooted to be free of each other. There are various components which influence abrasive wear and therefore the way of material removal. A small number of unique components have been proposed to illustrate the way where the outer material is eliminated.
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Figure 1.
Abrasive wear of industrial parts.
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Khanam et al. [1] investigated about the abrasive wear resistance of CNF enforced epoxy nanocomposites at different percentage of CNF concentration. It has been observed (Figure 2) that the neat epoxy composite revealed deep plowing line, many microcracks and surface covered with wear debris of detached matrix over the entire worn surface.
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Figure 2.
SEM image of worn surface after abrasive wear test of (a) neat epoxy, (b) 0.5 wt% CNF, (c) 1.0 wt% CNF, (d) 1.5 wt% CNF, (e) 2.0 wt% CNF and (f) 2.5 wt% CNF [1].
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3.2 Adhesive wear
\n
When one surface slides over the other interaction between the high spots produces occasional particles of wear debris. Mild adhesion is the expulsion of films, for example, oxides at a lower rate. Severe adhesion is the evacuation of metal because of tearing, breaking, and liquefying of metallic intersections (Figure 3). This prompts scraping or annoying of the surfaces and even seizure.
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Figure 3.
Adhesive wear in industries.
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Adhesive wear can be found between surfaces during frictional contact and by and large alludes to undesirable dislodging and connection of wear debris and material mixes starting with one surface then onto the next. Two glue wear types can be recognized.
Adhesive wear is brought about by relative movement, “direct contact” and plastic deformation which make wear debris and material transfer starting with one surface then onto the next.
Cohesive adhesive load, holds two surfaces together despite the fact that they are isolated by a quantifiable separation, with or with no real exchange of material. By and large, glue wear happens when two bodies slide over or are squeezed into one another, which advance material exchange. This can be depicted as plastic distortion of little pieces inside the surface layers. The asperity or minute high focuses (surface roughness) found on each surface influence the seriousness of how sections of oxides are pulled off and added to the next surface, mostly because of solid adhesive force between atoms [2] yet in addition because of collection of vitality in the plastic zone between the severities during relative movement.
\n\n
Yunxia et al. [3] investigated about the adhesive wear phenomena of aero-hydraulic spool valves and the investigation revealed the trimming and transformation of outer material due to the shear fracture of the bonded areas (Figure 4). It has been also claimed that the above mentioned work is an evidence of the adhesion wear process between spool and valve sleeve.
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Figure 4.
SEM morphology of adhesive wear surface of spool shoulder [3].
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3.3 Fatigue wear
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Surfaces can wear by fatigue when they are subject to fluctuating loads. High surface stresses cause cracks to spread into the material, and when two or more of these cracks become joined together large loose particles are formed. Thermal Surface Fatigue occurs when high repetitive stresses are generated through the heating caused by the contact of the two contacting components which result in cracking of the surface and the loss of small chunks of material. Surface fatigue is a cycle where the outside of a material is debilitated by cyclic stacking, which is one sort of broad material weariness (Figure 5). Fatigue wear is developed when the wear particles are confined by cyclic split development of microcracks on a superficial level. These microcracks are either shallow splits or subsurface breaks.
\n
Figure 5.
Fatigue and pitting wear in industrial parts.
\n
Mao et al. [4] investigated the fatigue wear phenomena of the gear and in his investigation he found out that the main reason of fatigue wear is the high stress concentration. The pitting failure due to the stress concentration is illustrated in Figure 5.
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3.4 Fretting wear
\n
Fretting occurs where two contacting surfaces, often nominally at rest, undergo minute oscillatory tangential relative motion (Figure 6). Small particles of metal are removed from the surface and then oxidized. Typically occurs in bearings although the surfaces are hardened to compensate this problem and also can occur with cracks in the surface (fretting fatigue). This carries the higher risk of the two as can lead to failure of the bearings. Fretting wear is the rehashed recurrent scouring between two surfaces. Over some stretch of time fretting this will eliminate material from one or the two planes in contact. It happens normally in orientation, albeit most headers have their surfaces hardened to oppose the issue. Another issue happens when splits in either surface are made, known as fretting fatigue. It is the more genuine of the two marvels since it can prompt disastrous disappointment of the bearing. A related issue happens when the little particles eliminated by wear are oxidized in air. The oxides are generally harder than the fundamental metal, so wear quickens as the harder particles rub the metal surfaces further. Fretting corrosion acts similarly, particularly when water is available. Unprotected bearings on enormous structures like bridges can endure genuine debasement in conduct, particularly when salt is utilized during winter to deice the highways conveyed by the bridges. The issue of fretting corrosion was associated with the Silver Bridge misfortune and the Mianus River Bridge mishap.
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Figure 6.
Fretting wear in industrial parts.
\n
Akhtar et al. [5] revealed in his research that the surface after 300 N testing have very heavy plowing of the steel matrix (Figure 6). At higher loads microplowing is very severe and causes the rapid removal of the material from the surface of the composite.
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3.5 Erosive wear
\n
Erosive wear is loss of material from a solid surface due to relative motion in contact with a fluid which contains solid particles impingement by a flow of sand, or collapsing vapor bubbles (Figure 7). Erosive wear closely depends on the material properties of the particles, such as hardness, impact velocity, shape and impingement angle. Example: A common example is the erosive wear associated with the movement of slurries through piping and pumping equipment. Erosive wear can be characterized as an amazingly short sliding movement and is executed inside a brief timeframe stretch. Erosive wear is brought about by the effect of particles of solid or fluid against the surface. The affecting particles steadily eliminate material from the surface through rehashed deformation and cutting mechanisms. It is a broadly experienced system in industry. Because of the idea of the passing on measure, funneling frameworks are inclined to wear when rough particles must be moved. The pace of erosive wear depends upon various elements. The material qualities of the particles, for example, their shape, hardness, impact speed and impingement edge are essential factors alongside the properties of the surface being disintegrated. The impingement point is one of the most significant factors. For ductile materials, the greatest wear rate is discovered roughly at 30° impingement angle, while for brittle materials the most extreme wear rate happens when the impingement angle is normal to the surface.
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Figure 7.
Erosion of compressor blades in gas turbine engine.
\n
Swain et al. [6] investigated about the erosion behavior of the plasma sprayed NITINOL coating. In this work, the surface was eroded by 45 and 90° impingement angle of erodent. The wear mechanisms can be observed from the Figure 8. The surface impinged at 45° impingement angle (Figure 8(a)–(c)) having crater formation, chip formation and cutting grooves mechanisms. Whereas, the eroded surface at 90° impingement angle (Figure 8(d)–(f)) having crater formation, plastic deformation and lip formation mechanisms.
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Figure 8.
SEM morphologies of eroded surface at (a), (b), (c) 45° and (d), (e), (f) 90° impingement angle [6].
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3.6 Corrosive and oxidation wear
\n
Corrosion and oxidation wear happens both in oily and dry contacts (Figure 9). The essential reason are chemical reactions between weared surface and the eroding medium. Wear brought about by a synergistic activity of tribological stresses and consumption is likewise called tribocorrosion. Corrosive wear is otherwise called chemical wear. Corrosive wear is an assault on a material surface inside its condition. Corrosive wear can be either is wet or dry, contingent upon the sort of condition present for a specific response. Generally, wet erosion happens in an answer, for example, water, with some disintegrated species in it, which makes an acidic situation and response over the surface. Dry erosion is predominantly obstructed by the presence of dry gases, for example, characteristic air and nitrogen, etc. Since nature assumes an enormous function in corrosion wear, material choice is fundamental and ought to be the concentration before planning a segment. In erosion wear, corrosion and wear are two free instruments; if the demonstrations happen independently, the condition might be more basic than the consolidated impact of both. In presence of oil on a superficial level, consumption will be uniform all through the surface. On the off chance that limits of precious stone materials are defenseless to consumption rather than inside material, it is known as intergranular erosion. Pitting brought about by impingement of particles on the material surfaces produces pits and openings on the surfaces, which is difficult to perceive on a superficial level. Subsurface corrosion is disconnected particles that exist underneath the eroding material, essentially because of the response of constituents with the defused medium.
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Figure 9.
Corrosive and oxidation wear of structural members of industries.
\n
Akonko et al. [7] investigated the corrosive wear phenomena on both the protected and unprotected samples in the NaCl solution under a force of 5 N and found that the worn surface of a non-protected sample (Figure 10) indicated less cracks than those of cathodically protected (Figure 11). This indicates that the cathodic protection caused hydrogen embrittlement, and this has further boosted by stress, therefore caused more wear.
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Figure 10.
SEM images of the wear track on an unprotected sample in the NaCl solution: (a) wear track, (b) a closer view at the wear track.
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Figure 11.
SEM images of the wear track on a cathodically protected (−0.50 V) sample in the NaCl solution: (a) wear track, (b) a closer view at the wear track [7].
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4. Wear mechanisms
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\n
4.1 Adhesive wear
\n
The sort of mechanism (Figure 12) and the abundancy of surface fascination fluctuates between various materials yet are enhanced by an expansion in the thickness of “surface energy”. Most solids will stick on contact somewhat. Nonetheless, oxidation films, oils and contaminants normally happening for the most part stifle attachment, and unconstrained exothermic chemical reactions between surfaces by and large produce a substance with low vitality status in the retained species.
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Figure 12.
Adhesive wear mechanism.
\n
Adhesive wear can prompt an expansion in harshness and the production of projections (i.e., protuberances) over the first surface. In modern assembling, this is alluded to as irking, which inevitably penetrates the oxidized surface layer and interfaces with the fundamental mass material, improving the opportunities for a more grounded bond and plastic flow around the knot.
\n
A model for the wear volume for cement wear, V, can be portrayed by:
\n
\n\nV\n=\nK\n×\nW\nL\n/\nHv\n\n
\n
Where, ‘W’ represents load, ‘K’ is the wear coefficient, ‘L’ represents the sliding distance, and ‘Hv’ is the hardness.
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4.2 Abrasive wear
\n
The system of material expulsion in abrasive wear is essentially equivalent to machining and grinding during an assembling cycle (Figure 13). At the beginning of wear, the hard severities or particles enter into the milder surface under the typical contact tension. The wear trash regularly has a type of micro cutting chips.
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Figure 13.
Abrasive wear mechanism.
\n
A few methods have been suggested to foresee the volume misfortune in abrasive wear. A least difficult one includes the scratching of materials by angular shaped hard particles (indenter). Under an applied heap of P, the hard molecule enters the material surface to a profundity of h which is straightly relative to the applied burden (P) and conversely corresponding to the hardness (H) of the surface being scraped. As sliding happens, the molecule will furrow (cut) the surface delivering a depression, with the material initially ready being eliminated as wear flotsam and jetsam. On the off chance that the sliding distance (L) and the wear volume (V) can be written as:
\n
\n\nV\n=\nk\n.\n\nPL\nH\n\n\n
\n
Here, ‘k’ is wear coefficient partially reflecting the effects of geometries, and properties of the particles (or asperities), and partly reflecting the influences of additional factors such as sliding speed, and lubrication environments.
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\n
\n
4.3 Fatigue wear
\n
Two mechanisms (Figure 14) of fatigue wear are recognized: high-and low-cycle fatigue. In high-cycle fatigue, the quantity of cycles before fatigue is high, so the part life is generally long. The splits for this situation are created because of prior miniature imperfections in the material, near which the nearby pressure may surpass the yield esteem, despite the fact that ostensibly the naturally visible contact is in the flexible system. Gathering of plastic strain around inhomogeneities is an antecedent for commencement of a split. In the low-cycle fatigue, the quantity of cycles before disappointment is low, so the part bombs quick. In this mode, pliancy is prompted each cycle and the wear molecule is produced throughout aggregated cycles. The wear garbage is not produced at the principal cycles, yet just the shallow furrows because of plastic misshapening are framed, as talked about in. After a basic number of cycles, the plastic strain surpasses a basic worth and the crack happens. There are the three phases in break proliferation: split inception, development and post-basic stage, when the calamitous disappointment happens. The vast majority of the lifetime of the part is involved by the primary stage, with the spans of introductory splits around 2–3 μm and lower.
\n
Figure 14.
Fatigue wear mechanism.
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\n
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4.4 Fretting wear
\n
Cyclic motion between contacting surfaces is the essential ingredient in all types of fretting wear. It is a combination process that requires interaction of two surfaces, and exposed to minor amplitude of oscillations.
\n
According to the material properties of surfaces, adhesive, two-body abrasion and/or solid particles may produce wear debris. Wear particles detach and become comminuted (crushed) and the wear mechanism (Figure 15) changes to three-body abrasion when the work-hardened debris starts removing metal from the surfaces.
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Figure 15.
Fretting wear mechanism.
\n
Fretting wear arises as a result of the following order of events:
The normal load causes asperities to stick and the tangential oscillatory motion shaves the asperities and produces wear debris that stores.
The surviving (harder) asperities eventually act on the smooth surfaces causing them to undergo plastic deformation, create voids, propagate cracks and shear off sheets of particles which also gather in depressed areas of the surfaces.
Once the particles have accumulated sufficiently to span the gap among the surfaces, abrasion wear follows and the wear zone extents laterally.
As adhesion, delamination, and abrasion wear lasts, wear debris can no longer be contained in the primary zone and it outflows into surrounding valleys.
Because the maximum stress is at the center, the geometry becomes curved, micropits form and these coalesce into larger and deeper pits. Finally, depending on the displacement of the tangential motion, worm tracks or even big cracks can be produced in one or both surfaces.
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4.5 Corrosive and oxidation wear
\n
Metal surface is normally covered with a layer of oxide, which could restrict metal-to-metal interaction, and therefore evading the development of adhesion and reducing the tendency of adhesive wear. In this connection, oxide is a favorable factor in reducing wear rate of metallic materials. However, whether such beneficial effect can be realized or not, is intensely reliant on the material properties and on contact conditions. When the hardness of the metal underlying an oxide layer is low, or when the contact load is relatively higher, the metal beneath the oxide layer will deform plastically, and asperities in the rigid surface will penetrate through the thin oxide layer, leading to the normal metal-to-metal contact. In such case, wear by abrasion or adhesion will occur depending on the mechanical properties and chemical properties of the contacting metals. The beneficial effect of oxide is minimal and wear rate is generally high. On the other hand, when the underlying metal is hard enough to support the oxide film, such as on a surface engineered hard surface, a process known as oxidation wear (Figure 16) will occur.
\n
Figure 16.
Corrosive wear mechanism.
\n
It needs to be mentioned that during sliding, the increased surface temperature promoted by frictional heating, and the less activation energy of oxide formation caused by plastic deformation, can increase the oxidation rate. Thus, rapid oxidation can be achieved, and the oxide layer can grow thicker during sliding than that under static conditions. This ensures the fresh metal is rapidly covered with a new layer of oxide after the original oxide film was worn away. Oxidation wear will not happen in vacuum or in inert atmosphere, since re-oxidation is not possible. Oxidation is a minor form of wear. When the predominant wear mechanism is changed from abrasive or adhesive to oxidation wear, degree of wear can be reduced by some orders of magnitude.
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5. Use of surface coating for the protection from wear
\n
As wear is a surface or near surface phenomenon it has long been realized that the wear resistance of a component can be improved by providing a surface of different composition from the bulk material. After a brief introductory chapter wear phenomena and the properties required from a coating are addressed. Coating processes provide protection to a specific part or area of a structure exposed to harsh and corrosive environments in different fields ranging from aerospace and the automotive industry to tiny biomedical devices and implants inside the human body.
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\n
\n
6. Types of surface coating
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\n
6.1 Physical vapor deposition (PVD) coating
\n
PVD process is well-known for offering corrosion, wear resistance, and thin protective films on the surface of the materials that are exposed to corrosive media, and its applications range from decorative objects to industrial parts. The benefit of this technique is that the mechanical, corrosion, and esthetic properties of the coating layers could be adjusted on demand. Generally, PVD is a method that occurs in a high vacuum, and the solid/liquid materials transfer to a vapor phase followed by a metal vapor condensation, which creates a solid and thick film. The common types of PVD methods are sputtering and evaporation. Since the coating layers created by PVD are thin in nature, there is always a need for multilayered coatings while the materials selection should be considered carefully.
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\n
6.2 Chemical vapor deposition (CVD) coating
\n
Another type of vapor deposition is called CVD. This process undergoes a high vacuum and is widely used in the semiconductors industry providing a solid, high quality, and a high resistance coating layer on any substrate. CVD can be used for mechanical parts in continuous interaction, which need protection for corrosion and wear. In this method, the substrate, known as a wafer, would be exposed to a set of volatile material precursors where a chemical reaction creates a deposition layer on the surface of the material. However, some by products of these chemical reactions, which are removed by continuous airflow of the vacuum pump, can stay in the chamber.
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\n
\n
6.3 Micro-arc oxidation (MAO) coating
\n
MAO method is known as a flexible method of coating concerning the composition of coatings. In general, MAO utilizes a high voltage difference between anode and cathode to generate micro-arcs as plasma channels. When these arcs hit the substrate, they melt a portion of the surface, depending on the intensity of the micro-arcs. Simultaneously, plasma networks discharge their pressure, which supports the deposition of coating materials in the working electrolyte on the substrate surface. The existing oxygen in the electrolyte causes a chemical reaction resulting oxidation and the oxides gets deposited on the surface of the substrate. The adaptability of this process lies in the flexibility of combining preferred elements and compounds as a solute in the working electrolyte. With MAO, the most common substrate materials are Al, Mg, Ti, and their alloys.
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\n
\n
6.4 Electro deposition coating
\n
Electro deposition of materials is considered a type of protection utilizing the deposition of metallic ions on a coating substrate. In this method, a difference in potential between anode and cathode poles causes an ion transfer in the unit cell. After a while, a coating layer forms on the submerged sample by getting ions from the other electrode. The common group of metals that have been intensively studied includes, but is not limited to, Ni-P, Ag/Pd, Cu/Ag, Cu/Ni, and Co/Pt.
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\n
\n
6.5 Sol-gel coating
\n
Sol–gel synthesis is used to obtain coatings that can modify the surfaces of metals to avoid corrosion or to enhance the biocompatibility and bioactivity of metals and their alloys that are of biomedical interest. Anticorrosion coatings composed of smart coatings and self-healing coatings will be described.
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\n
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6.6 Thermal spray coating
\n
Thermal spray coating is a general term for a series of processes that utilize a plasma, electric, or chemical combustion heat source to melt a set of designed materials and spray the melt on the surface in order to produce a protective layer. These are reliable types of corrosion- and wear-resistant coatings. In this process, a heat source or plasma, heats up the coating materials to a fully molten or semi-molten phase and sprays them on the substrate material with a high velocity jet.
\n
Thermal spraying dates back to the early 1900s when Dr. Schoop [1] first carried out experiments in which molten metal were atomized by a stream of high-pressure gas and propelled on to a surface. The Schoop process consisted of a crucible filled with molten metal while the propellant, hot compressed air, provided enough pressure to break up the molten metal, creating a spray jet. This system was quite rudimentary and inefficient. Following Schoop’s work some improvements to the process were introduced. But the disadvantages of the process is that, it was only useful for low-melting-temperature metals, that the molten metal caused severe corrosion and that it was not possible to establish a continuous process, were enough to stop further progress.
\n
Schoop then focused his efforts in another direction and in 1912 the first device for spraying metal wires was produced. The principle of this process is simple; a wire was fed into a combustion flame which melted the tip of the wire and then compressed air surrounding the flame atomized the molten metal and drove the tiny droplets on to a substrate to form a coating. In addition to improvements to nozzle and gun design along with the wire feed drive rolls, the basic principle of the process is the same today. This procedure is called flame spraying (FS) and covers an enormous group of thermal spray techniques which use powder, wires or rods.
\n
A completely new concept in thermal spraying was introduced by Schoop in 1914 when he used electricity to melt the feedstock material. The most advanced equipment made by Schoop was quite similar to current electric arc spraying. This method is based on producing an electric arc among two wires of conducting materials, which are fed together inside the gun. This arc is created at the tip of the wires and a jet of compressed air propels the molten metal to the substrate.
\n
The concept of powder FS was introduced by F. Schori in the early 1930s, when a metallic powder was fed into a flame by the Venturi effect. The coating powder was heated in the nozzle and the exhaust gases (oxygen and acetylene) propelled the droplets. Improvements to the process incorporated in modern guns include an inert compressed gas that pressurizes the combustion chamber and results in rise in particle velocity.
\n
The main problem associated with these early techniques was feedstock material. They all used a low-melting-point material, which leads to limited applications. Years passed, and the demand for high-temperature-resistant materials increased, until in the 1950s new systems that would boost the thermal spray market appeared. Firstly a modification of wire FS, the ceramic rod FS technique, which could use stabilized zirconias and aluminas appeared. However, it was the development, in about 1955, of the detonation gun (D-Gun) and atmospheric plasma spraying (APS) in about 1960 that proved to be the watershed as regards thermal spray applications.
\n
The thickness achieved in thermal spray coating techniques can range from 20 micron to several milli meters which are significantly higher than the thickness offered by electroplating, CVD, or PVD processes. In addition, the materials that can be used as feedstock of thermal spray coatings range from refractory metals and metallic alloys to ceramics, plastics, and composites and can easily cover a relatively high surface area of a substrate. Therefore the current chapter will mostly focus on this coating process.
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\n
\n
\n
7. Types of thermal spray processes
\n
There are various types of thermal spray coating processes introduced by the researchers (Figure 17).
\n
Figure 17.
Classification of thermal spray coating process.
\n
\n
7.1 Powder flame spraying
\n
In powder flame spraying, the feedstock material is injected to the plume for heating and melted by the heating zone. After melting the molten particles are propagated towards the substrate surface. Then the molten particles are deposited on the substrate surface or pre-deposited splat to form a coating (Figure 18). The molten particles are ejected by the flame spray gun. The only difference between powder flame spraying and wire flame spraying is the feedstock material.
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Figure 18.
Powder flame spray technology.
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\n
\n
7.2 Wire or rod flame spraying
\n
In rod type flame spray, the rod or wire is allowed to the heating zone where it melts and propagated by the plume towards the substrate to form coating (Figure 19). The feedstock rod may be a conventional rod or wire or manufactured by powder metallurgy process (sintering or binding). The melted particles are propelled towards the substrate, strike the surface at high velocity and flatten and form coating with a high adhesion strength with previously formed splat and substrate.
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Figure 19.
Flame wire spray technology.
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\n
\n
7.3 Detonation flame spraying
\n
By the term “detonation” is meant a very rapid combustion in which the flame front moves at velocities higher than the velocity of sound in the unburned gases, and therefore characterized as supersonic velocities. A precisely measured quantity of the combustion mixture consisting of oxygen and acetylene is fed through a tubular barrel closed at one end. In order to prevent the possible back firing a blanket of nitrogen gas is allowed to cover the gas inlets. Simultaneously, a predetermined quantity of the coating powder is injected into the combustion chamber. The gas mixture inside the chamber is ignited by a simple spark plug. The gas mixture combustion generates plume which melt the particles to form coating (Figure 20).
\n
Figure 20.
Detonation flame spray technology.
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\n
\n
7.4 High velocity oxy-fuel spraying
\n
High velocity powder flame spraying was developed about 1981 and comprises a continuous combustion procedure that produces exit gas velocities estimated to be 4000–5000 feet per second. This is accomplished by burning a fuel gas (usually propylene) with oxygen under high pressure (60–90 psi) in an internal combustion chamber. Hot exhaust gases are discharged from the combustion chamber through exhaust ports and thereafter expanded into an extending nozzle. Powder is fed axially into this nozzle and confined by the exhaust gas stream until it exits in a thin high speed jet to produce coatings which are much denser than those produced with conventional or standard powder flame spraying techniques (Figure 21).
\n
Figure 21.
HVOF spray technology.
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\n
\n
7.5 Wire arc spraying
\n
Twin wire arc spraying is the most economical thermal spraying process. In this type of spraying process the heating and melting occur when two oppositely charged wires are fed together in a way that arc is generated at their intersection (Figure 22). Once struck, the arc continuously melts the wires, and compressed air blown directly behind the point of contact, atomizes and projects the molten droplets, which sticks to the substrate to form a coating. Arc fluctuations due to periodic removal of molten droplets from the electrode tips have strong effects on melting and coating properties such as porosity, microstructure and oxide content.
\n
Figure 22.
Wire arc spray technology.
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\n
\n
7.6 Plasma spraying process
\n
Plasma spraying is a flexible and low-cost method to manufacture coating and bulk materials. The first idea of a plasma spray process was patented in 1909 in Germany, and the first structural plasma installation appeared in the 1960’s, as the product of two American companies Plasmadyne and Union Carbide. A gas, usually argon, but occasionally including nitrogen, hydrogen, or helium, is allowed to flow between a tungsten cathode and a water-cooled copper anode. The cathode is placed in the cylindrical nozzle and the cylindrical nozzle is the anode. An electric arc is initiated between the two electrodes using a high frequency discharge and then sustained using dc power. The plasma is generated by the ionization of gas by the arc. The feedstock materials injected through the gun nozzle into the plasma plume, where it is melted and propagated to the substrates (Figure 23) [2, 6, 8, 9, 10, 11, 12].
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Figure 23.
Plasma spray coating technology.
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\n
\n
\n
8. Application of thermal spray technology for the protection from wear
\n
A large range of industrial parts get advantage from thermal spraying, whether it is a portion of the manufacturing processes or as reclamations or re-engineering techniques. Some materials are used for minute role applications and others are sprayed by the tonne. Every application utilizes an amalgamation of procedure and material to give in the desired profit.
\n
Reclamation and re-engineering of a wide range of rotating and moving parts from machines of all kinds, including: vehicles of both railways and highways, ships, aerospace, printing industries, paper industries, chemical industries, food industries, mining, earthmovers, machine tools, landing gear (chrome replacement) and any apparatus which is subject to wear, erosion or corrosion. This is done using either arc spray, flame spray or HVOF systems to spray steels, nickel alloys, carbides, stainless alloys, bronzes, copper and many other materials. New components which benefit from the enhanced surface properties that thermal spraying provides, include: Gate and ball valves, rock drilling bits, and down hole tools, print rollers, fluid seals, aerospace combustion chambers, turbine blades. Thermal sprayed coatings are used on a vast range of components which operate in harsh surroundings where, erosion, wear, corrosion or high temperature reduce part life. Part life is significantly prolonged due to thermal spray processes.
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\n
\n
9. Conclusions
\n
\n
Wear kinds of adhesive, abrasive, fatigue, and tribochemical wear are presented and their wear instruments are clarified with wear models in this chapter. In real wear of triboelements, a portion of these wear types are included simultaneously, and significant wear type changes at times starting with one then onto the next during running because of wear itself.
Then again, wear is delicate to the difference in different framework boundaries, for example, mass, shape, stiffness, material properties, and condition. In light of such multiparameter affectability of wear, quantitative expectation of wear rate is still a long way from the real world.
It gets significant, thusly, to perceive the significant wear type and its ordinary wear mechanisms according to framework boundaries.
Surface covering improves the life of the segment and lessens the expense of substitution. The motivation behind surface innovation is to deliver practically compelling surfaces. A wide scope of coatings can improve the consumption, disintegration and wear obstruction of materials.
We can reason that thermal spray coating is one of the most significant strategies of the surface change strategy. This examination was a push to give essential data with respect to a portion of the fundamental thermal spray strategies among which HVOF covering measure is most appropriate.
By utilizing HVOF spray method uniform covering thickness, nonstop layer of covering and high hardness can be acquired. It has more favorable circumstances over the high quality, hardness, porosity, wear and erosion when contrasted with different cycle.
\n\n
\n\n',keywords:"wear, type of wear, tribology, surface coating, thermal spray coating",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/73685.pdf",chapterXML:"https://mts.intechopen.com/source/xml/73685.xml",downloadPdfUrl:"/chapter/pdf-download/73685",previewPdfUrl:"/chapter/pdf-preview/73685",totalDownloads:111,totalViews:0,totalCrossrefCites:0,dateSubmitted:"August 2nd 2020",dateReviewed:"September 27th 2020",datePrePublished:"December 16th 2020",datePublished:"February 3rd 2021",dateFinished:"October 20th 2020",readingETA:"0",abstract:"Wear is the damaging, gradual removal or deformation of material at solid surfaces. Causes of wear can be mechanical or chemical. The study of wear and related processes is known as tribology. Abrasive wear alone has been estimated to cost 1–4% of the gross national product of industrialized nations. The current chapter focuses on types of wear phenomena observed in the industries (such as abrasive wear, adhesive wear, fretting wear, fatigue wear, erosive wear and corrosive wear), their mechanisms, application of surface coating for the protection of the surface from the industrial wear, types of surface coatings, thermal spray coating, types of thermal spray coating and its application in industry to protect the surface from wear. The detail information about the wear phenomena will help the industries to minimize their maintenance cost of the parts.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/73685",risUrl:"/chapter/ris/73685",signatures:"Biswajit Swain, Subrat Bhuyan, Rameswar Behera, Soumya Sanjeeb Mohapatra and Ajit Behera",book:{id:"9865",title:"Tribology in Materials and Manufacturing",subtitle:"Wear, Friction and Lubrication",fullTitle:"Tribology in Materials and Manufacturing - Wear, Friction and Lubrication",slug:"tribology-in-materials-and-manufacturing-wear-friction-and-lubrication",publishedDate:"February 3rd 2021",bookSignature:"Amar Patnaik, Tej Singh and Vikas Kukshal",coverURL:"https://cdn.intechopen.com/books/images_new/9865.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"43660",title:"Associate Prof.",name:"Amar",middleName:null,surname:"Patnaik",slug:"amar-patnaik",fullName:"Amar Patnaik"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"326892",title:"Ph.D.",name:"Biswajit",middleName:null,surname:"Swain",fullName:"Biswajit Swain",slug:"biswajit-swain",email:"biswajitnitrkl@gmail.com",position:null,institution:null},{id:"329211",title:"Mr.",name:"Rameswar",middleName:null,surname:"Behera",fullName:"Rameswar Behera",slug:"rameswar-behera",email:"apnitrkl92@gmail.com",position:null,institution:{name:"National Institute of Technology Rourkela",institutionURL:null,country:{name:"India"}}},{id:"329212",title:"Dr.",name:"Soumya Sanjeeb",middleName:null,surname:"Moahapatra",fullName:"Soumya Sanjeeb Moahapatra",slug:"soumya-sanjeeb-moahapatra",email:"pmnitrkl92@gmail.com",position:null,institution:{name:"National Institute of Technology Rourkela",institutionURL:null,country:{name:"India"}}},{id:"329213",title:"Dr.",name:"Ajit",middleName:null,surname:"Behera",fullName:"Ajit Behera",slug:"ajit-behera",email:"biswajitswain169@gmail.com",position:null,institution:{name:"National Institute of Technology Rourkela",institutionURL:null,country:{name:"India"}}}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Industrial wear problems",level:"1"},{id:"sec_3",title:"3. Types of wear",level:"1"},{id:"sec_3_2",title:"3.1 Abrasive Wear",level:"2"},{id:"sec_4_2",title:"3.2 Adhesive wear",level:"2"},{id:"sec_5_2",title:"3.3 Fatigue wear",level:"2"},{id:"sec_6_2",title:"3.4 Fretting wear",level:"2"},{id:"sec_7_2",title:"3.5 Erosive wear",level:"2"},{id:"sec_8_2",title:"3.6 Corrosive and oxidation wear",level:"2"},{id:"sec_10",title:"4. Wear mechanisms",level:"1"},{id:"sec_10_2",title:"4.1 Adhesive wear",level:"2"},{id:"sec_11_2",title:"4.2 Abrasive wear",level:"2"},{id:"sec_12_2",title:"4.3 Fatigue wear",level:"2"},{id:"sec_13_2",title:"4.4 Fretting wear",level:"2"},{id:"sec_14_2",title:"4.5 Corrosive and oxidation wear",level:"2"},{id:"sec_16",title:"5. Use of surface coating for the protection from wear",level:"1"},{id:"sec_17",title:"6. Types of surface coating",level:"1"},{id:"sec_17_2",title:"6.1 Physical vapor deposition (PVD) coating",level:"2"},{id:"sec_18_2",title:"6.2 Chemical vapor deposition (CVD) coating",level:"2"},{id:"sec_19_2",title:"6.3 Micro-arc oxidation (MAO) coating",level:"2"},{id:"sec_20_2",title:"6.4 Electro deposition coating",level:"2"},{id:"sec_21_2",title:"6.5 Sol-gel coating",level:"2"},{id:"sec_22_2",title:"6.6 Thermal spray coating",level:"2"},{id:"sec_24",title:"7. Types of thermal spray processes",level:"1"},{id:"sec_24_2",title:"7.1 Powder flame spraying",level:"2"},{id:"sec_25_2",title:"7.2 Wire or rod flame spraying",level:"2"},{id:"sec_26_2",title:"7.3 Detonation flame spraying",level:"2"},{id:"sec_27_2",title:"7.4 High velocity oxy-fuel spraying",level:"2"},{id:"sec_28_2",title:"7.5 Wire arc spraying",level:"2"},{id:"sec_29_2",title:"7.6 Plasma spraying process",level:"2"},{id:"sec_31",title:"8. Application of thermal spray technology for the protection from wear",level:"1"},{id:"sec_32",title:"9. Conclusions",level:"1"}],chapterReferences:[{id:"B1",body:'\nKhanam A, Mordina B, Tiwari RK. Statistical evaluation of the effect of carbon nanofibre content on tribological properties of epoxy nanocomposites. J Compos Mater. 2015;49(20): 2497-507.\n'},{id:"B2",body:'\nSwain B, Bajpai S, Behera A. Microstructural evolution of NITINOL and their species formed by atmospheric plasma spraying. Surf Topogr Metrol Prop [Internet]. 2018;7(1):015006. Available from: https://doi.org/10.1088/2051-672X/aaf30e\n\n'},{id:"B3",body:'\nYunxia C, Wenjun G, Rui K. Coupling behavior between adhesive and abrasive wear mechanism of aero-hydraulic spool valves. Chinese J Aeronaut [Internet]. 2016;29(4):1119-31. Available from: http://dx.doi.org/10.1016/j.cja.2016.01.001\n\n'},{id:"B4",body:'\nMao K. Gear tooth contact analysis and its application in the reduction of fatigue wear. Wear. 2007;262(11-12):1281-8.\n'},{id:"B5",body:'\nAkhtar F, Guo SJ. Microstructure, mechanical and fretting wear properties of TiC-stainless steel composites. Mater Charact. 2008;59(1):84-90.\n'},{id:"B6",body:'\nSwain B, Mallick P, Bhuyan SK, Mohapatra SS, Mishra SC, Behera A. Mechanical Properties of NiTi Plasma Spray Coating. J Therm Spray Technol [Internet]. 2020 Apr 16;29(4):741-55. Available from: http://link.springer.com/10.1007/s11666-020-01017-6\n\n'},{id:"B7",body:'\nAkonko S, Li DY, Ziomek-Moroz M. Effects of cathodic protection on corrosive wear of 304 stainless steel. Tribol Lett. 2005;18(3):405-10.\n'},{id:"B8",body:'\nSwain B, Patnaik A, Bhuyan SK, Barik KN, Sethi SK, Samal S, et al. Solid particle erosion wear on plasma sprayed mild steel and copper surface. In: Materials Today: Proceedings. 2018.\n'},{id:"B9",body:'\nBiswajit Swain, Swadhin Patel, Priyabrata Mallick, Soumya Sanjeeb Mohapatra AB. Solid particle erosion wear of plasma sprayed NiTi alloy used for aerospace applications. In: ITSC 2019—Proceedings of the International Thermal Spray Conference. 2019. p. 346-51.\n'},{id:"B10",body:'\nMallick P, Behera B, Patel SK, Swain B, Roshan R, Behera A. Plasma spray parameters to optimize the properties of abrasion coating used in axial flow compressors of aero-engines to maintain blade tip clearance. Mater Today Proc [Internet]. 2020 May; Available from: https://linkinghub.elsevier.com/retrieve/pii/S2214785320328492\n\n'},{id:"B11",body:'\nKumar B, Soumya S, Mohapatra S, Power G. Sensitivity of Process Parameters in Atmospheric Plasma Spray Coating. J Therm Spray Eng. 2018;1(1):1-6.\n'},{id:"B12",body:'\nSwain B, Mallick P, Patel S, Roshan R, Mohapatra SS, Bhuyan S, et al. Failure analysis and materials development of gas turbine blades. Mater Today Proc [Internet]. 2020 Apr; Available from: https://linkinghub.elsevier.com/retrieve/pii/S2214785320316497\n\n'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Biswajit Swain",address:"biswajitnitrkl@gmail.com",affiliation:'
Department of Metallurgical and Materials Engineering, National Institute of Technology Rourkela, India
Department of Metallurgical and Materials Engineering, National Institute of Technology Rourkela, India
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