Methods of extraction of pectin from various agrowaste compounds.
\r\n\t
",isbn:"978-1-83968-856-0",printIsbn:"978-1-83968-855-3",pdfIsbn:"978-1-83968-857-7",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"c5a667ba20185b3a039de5c53772da49",bookSignature:"M.D. Angelo Guttadauro",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10316.jpg",keywords:"Causes of Acute Appendicitis, Risk Factors Appendicitis, Ultrasound in Appendicitis, Alvarado Score, Uncomplicated Appendicitis, Marker of Acute Appendicitis, Appendicectomy, Mini-invasive Appendicectomy, Perforated Appendicitis, Complicated Appendicitis, Appendicitis in Elderly, Appendicitis in Pregnancy",numberOfDownloads:54,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"September 17th 2020",dateEndSecondStepPublish:"October 15th 2020",dateEndThirdStepPublish:"December 14th 2020",dateEndFourthStepPublish:"March 4th 2021",dateEndFifthStepPublish:"May 3rd 2021",remainingDaysToSecondStep:"6 months",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:'Dr. Guttadauro is the founder and head of the "Hernia Center" of Monza-Brianza. In 2015 he obtained an international patent for a prosthesis for inguinal hernioplasty and standardized a new surgical technique for the application of the aforementioned method. He has presented his works at around 200 national and international congresses.',coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"239365",title:"M.D.",name:"Angelo",middleName:null,surname:"Guttadauro",slug:"angelo-guttadauro",fullName:"Angelo Guttadauro",profilePictureURL:"https://mts.intechopen.com/storage/users/239365/images/system/239365.jpeg",biography:'Dr Angelo Guttadauro is a researcher at the University of Milan-Bicocca and first level manager at the U.O.C. of General Surgery at the Zucchi Clinical Institutes of Monza. He is the founder and head of the \\"Hernia Center\\" of Monza-Brianza. He has participated in research projects of the Ministry of University and Scientific and Technological Research. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"72",title:"Ionic Liquids",subtitle:"Theory, Properties, New Approaches",isOpenForSubmission:!1,hash:"d94ffa3cfa10505e3b1d676d46fcd3f5",slug:"ionic-liquids-theory-properties-new-approaches",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/72.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"314",title:"Regenerative Medicine and Tissue Engineering",subtitle:"Cells and Biomaterials",isOpenForSubmission:!1,hash:"bb67e80e480c86bb8315458012d65686",slug:"regenerative-medicine-and-tissue-engineering-cells-and-biomaterials",bookSignature:"Daniel Eberli",coverURL:"https://cdn.intechopen.com/books/images_new/314.jpg",editedByType:"Edited by",editors:[{id:"6495",title:"Dr.",name:"Daniel",surname:"Eberli",slug:"daniel-eberli",fullName:"Daniel Eberli"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"57",title:"Physics and Applications of Graphene",subtitle:"Experiments",isOpenForSubmission:!1,hash:"0e6622a71cf4f02f45bfdd5691e1189a",slug:"physics-and-applications-of-graphene-experiments",bookSignature:"Sergey Mikhailov",coverURL:"https://cdn.intechopen.com/books/images_new/57.jpg",editedByType:"Edited by",editors:[{id:"16042",title:"Dr.",name:"Sergey",surname:"Mikhailov",slug:"sergey-mikhailov",fullName:"Sergey Mikhailov"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1373",title:"Ionic Liquids",subtitle:"Applications and Perspectives",isOpenForSubmission:!1,hash:"5e9ae5ae9167cde4b344e499a792c41c",slug:"ionic-liquids-applications-and-perspectives",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/1373.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"66671",title:"Extraction and Purification of Pectin from Agro-Industrial Wastes",doi:"10.5772/intechopen.85585",slug:"extraction-and-purification-of-pectin-from-agro-industrial-wastes",body:'\nPectins are complex branched polysaccharides present in the primary cell wall of plants [1]. It is a highly valued food ingredient commonly used as a gelling agent and stabilizer [2]. It is usually extracted by chemical or enzymatic methods from fruits [3]. Pectin is considered as the most complex macromolecule in nature, since it can be composed of up to 17 different monosaccharides containing more than 20 different linkages [4].
\nPectins are enriched with repeated units of methyl ester galacturonic acid [4]. They form chemically stable and physically strong skeletal tissues of plants when combined with proteins and other polysaccharides [5]. They are usually produced in the initial stages of primary cell wall growth and make one third of the cell wall in both monocots and dicots [6]. Pectin is significantly reduced or absent in non-extendable secondary cell walls and is the only major class of plant polysaccharide largely limited to primary cell walls [7]. Pectin imparts strength and flexibility to the cell wall, apart from number of fundamental biological functions such as signalling, cell proliferation, differentiation, cell adhesion and maintaining turgor pressure of cell [8]. Pectins are involved in regulating mobility of water and plant fluids through the rapidly growing parts [6]. It also influences the texture of fruit and vegetables [9]. Apple pomace and orange peel are the two major sources of commercial pectin due to the poor gelling behaviour of pectin from other sources [6].
\nPectin is one of the most important polysaccharides due to its increasing demand in the global market, reaching a total production capacity of around 45–50 Million tonnes per annum. While the demand in 2011 was approximately 140–160 Million tonnes per annum, earning the interest of industry in this complex polysaccharide processing [10]. Pectins have received considerable attention as a high fibre diet that benefits health by reducing cholesterol and, serum glucose levels and acting as anticancer agents [11]. Pectins have shown promising results as drug carriers for oral drug delivery and are widely used for various bio-medical applications [5]. In addition, pectin has been described as an emerging prebiotic with the ability to modulate colon microbiota [12]. Considering above properties and applications, pectin has gained immense priority in the global biopolymer market with great potential and opportunities for future developments.
\nOne of the most abundant macromolecules present in the primary cell wall of the plants is pectin; their presence is detected in the matrix as well as in the middle lamellae [7]. Pectin is highly rich with galacturonic acid (GalA), that forms the backbone of three more domains found along with pectin that are homogalacturonan (HGA), rhamnogalacturonan-I (RG-I) and rhamnogalacturonan-II (RG-II) [13]. About 70% of pectin is mainly composed of galacturonic acid (GA) [14]. Pectin is made of three polysaccharides that are covalently linked together, thus forming pectin networks in the cell wall matrix and the middle lamellae [15, 16].
\nHomogalacturonan (HG) takes up about 60–65% of the total pectin [3, 17], with a backbone of alpha-1,4-linked GalA residues, these GalA residues are methyl esterified which has an important role in the physical properties of pectin [4]. The presence of HG is seen to be present in approximately 100 GalA residues, but there are cases when its detected interspersed within other pectin polysaccharide [14]. On the other hand rhamnogalacturonan-I (RG-I) backbone which contributes 20–35% of pectin is composed of repeated and alternating groups of l-rhamnosyl and d-galacturonosyl residues [18]. There can be as many repeats as 300 of this disaccharide in case of sycamore cells, which are cultured in suspension [3, 16, 19]. The rhamnosyl residues have side chains of sugars which are mainly consisting of either galactosyl or arabinosyl residues [5]. The GalA residue of RGI unlike HGA are mostly not methyl esterified [20].
\nRhamnogalacturonan-II (RG-II) is one of the highly conserved and complex structure which consist of distinct regions within HG, which makes up about 10% of the pectin [3], they have side chains of four different types with a particular sugar residue like aceric acid, apiose-3-deoxy-lyxo-2-heptulosaric acid, and 3-deoxy-manno-2-octulosonic acid. The HG residues along with nine of the GalA residues are attached to these side chains [3, 5]. There are other substituted HG residues that make up pectin such as xylogalacturonan and apiogalacturonan whose expression is restriction. Even a minor mutation in R-II structure can lead to defects in the plant growth like dwarfism, thus suggesting its importance for normal growth of plant [3]. RG-I being highly branched in nature thus, called as the hairy region of pectin on the other hand HGA domain are known as the smooth region [7]. It is generally believed and noticed that there is covalent linkage within the pectin polysaccharides and pectin degrading enzymes are needed to separate and isolate HG, RG-I and RG-II from each other [21, 22]. Due to their similarity in HG and RG-II backbone structure composing of 1-4-linked alpha-D-GalA residues, they are likely to be linked covalently but there are no reports of RG-I to be covalently linked with HG [23].
\nPectin precipitates as a solid gel on treating with a dehydrating agent like alcohol. They are extremely sensitive to dehydration and get effected by any other hydrophilic colloids as well, thus they are known to be insoluble in most of the bio-colloids. The negative charge of pectin depends on the number of free carboxyl group that is mainly responsible for its precipitation [24].
\nBased on solubility pectins are of two types i.e., water soluble and water insoluble. Factors affecting the solubility of pectin are pH, temperature, nature of the solute and concentration of the solute [6, 13]. Pectin attains stability at a pH of 4 [17]. The solubility of pectin also depends on its composition like monovalent cation of pectin are soluble in water whereas di or trivalent are insoluble in water.
\nOne of the most interesting properties of pectin is its ability to form gel in the presence of either acid or calcium or sugar, this enables them to be used in many food industries [15]. Hydrogen bonding and hydrophobic interactions between polymer chains stabilizes the pectin polymer [9].
\nPectin is a high molecular weight polysaccharide that is present in almost all plants and help in maintaining the integrity of cell structure. Pectin is used in food industries to increase the viscosity of food products such as beverages, jams and jellies. It also has implications in pharmaceutical industry, especially in drug formulations, as an excipient due to its characteristics in release kinetics. Due to increased demand for pectin in food, pharmaceutical and therapeutic applications, thus, require efficient extraction processes. In order to increase the yield of pectin, various extraction methods have been adapted to obtain insoluble pectin present in the middle lamellae of plant cells, one of them being heating in acidic medium that makes insoluble pectin as soluble. Ripening of fruits also converts insoluble pectin into soluble pectin. Pectin can be extracted from various kinds of fruits, but the most commercial form of pectin is extracted from the peels of citrus fruits by alcohol precipitation [9, 25]. Citrus fruits contain 0.5–3.5% pectin which is largely present in the peel of fruits [26].
\nPectin has been isolated from various plants such as apple [27], citrus peel, carrots [28], sugar beet pulp [29, 30], sunflower heads [31], papaya [32] and oranges [33]. The most commonly used method for extracting pectin from plant tissue is by heating the plant sample in acidified water. The addition of extra chelating agents such as EDTA to the extraction mixture helps in easy release of pectin from cell wall. Care should be taken not to perform a long period of direct heating as it may lead to the thermal degradation of the polymer. Extraction process of pectin is carried out under reflux using acidified water at 97°C for 30 min. The hot acid extract was then filtered using a cheese cloth to remove the pulp. The filtrate was then cooled to 4°C and precipitated using double the volume of ethanol. The solvent precipitate mixture is then mixed till the pectin floats and removed by using cheese cloth followed by drying [27].
\nPectin is also extracted from dried sugar beet pulp after treating with acidified medium followed by purification through alcohol precipitation. Xin Huang et al., slightly modified the traditional method, where the sample was diluted with deionized water and was made acidic (pH −1.2) by using HCl. The sample was then heated to 90°C for 3 h and cooled to 40°C (pH −4.5) with 25 g/100 g ammonia. The mixture was then filtered using a Buchner funnel and pectin was precipitated using ethanol [29]. The ethanol is removed by squeezing with nylon cloth and washed several times followed by drying.
\nThe carrot pomace is also used for pectin extraction by treating with hot aqueous citric acid solution adjusted to the desired pH. The pectin yield was maximum at the following optimum conditions: pH −1.3; temperature 90°C; heating time 79.8 min. Under these conditions, the extraction yield of carrot pomace pectin was found to be 16.0%. The extract mixture was then allowed to cool, filtered and precipitated by using ethanol in the ratio 2:1 [28]. Dried papaya peel can be used in pectin extraction where the majority of the lipids, and soluble pigments are removed by treating with ethanol and acetone. It is repeatedly homogenised with 95% ethanol and filtered until the filtrate becomes clear. The final filtration was done with the residue homogenised in acetone and dried overnight to obtain the alcohol insoluble residue (AIR). The majority of the pectin in the papaya AIR is present as chelator soluble pectin (CSP) followed by sodium carbonate soluble pectin (SSP) and water-soluble pectin (WSP). The WSP fraction is first obtained from the AIR by boiling it in water and filtering it. The remaining residue is treated with 0.05 M cyclohexane trans-1,2-diamine tetra-acetic acid (CDTA) in 0.1 M potassium acetate (pH 6.5) for 6 h at 28°C and filtered to give the CSP fraction. The residue is then treated with 0.05 M sodium carbonate solution having 0.02 M NaBH4 for 16 h at 4°C, and subsequently for 6 h at 28°C. The solution when filtered gives the SSP fraction of the AIR [32].
\nAgro-industrial wastes can be used as the raw material for the production of industrial low and high methoxy pectin. The alcohol insoluble material (AIM) produced from dried agrowaste by boiling it with 3 volumes of ethanol for 25 min and continuous washing with 70% ethanol to remove impurities such as pigments, free sugars, etc. Sunflower heads also act as potential sources for pectin extraction. The heads are washed by hot distilled water through a mesh or cheese cloth and the pectin was precipitated by addition of 1 M nitric acid at 1:5 acid:filtrate ratio [34]. The mixture was maintained for 1 h at 5°C and was washed six times in ethanol solvent at 1:2 gel:solvent ratio to remove the impurities and to increase pH by removing the acid [31]. The washed pectin gel can be dried in a vacuum oven at 55°C for 16 h. The dried pectin flakes are ground into a powder for further use (Table 1).
\nMaterial | \nExtraction process | \nPectin (%) | \nReferences | \n
---|---|---|---|
Cacao pod husk ( | \nAcid extraction | \n3.7–8.6 | \n[34] | \n
Mangosteen rind ( | \nChemical treatment | \n23.5 | \n[35] | \n
Durian rind ( | \nAcid extraction | \n2.1–10.25 | \n[36] | \n
Orange peels ( | \nAcid extraction | \n0.2–6 | \n[37] | \n
Lemon peels ( | \nAcid extraction | \n0.8–8 | \n[37] | \n
Dragon fruit peels ( | \nUltrasound assisted | \n1.89–7.65 | \n[38] | \n
Banana-stem, leaf, peel ( | \nAlcohol precipitation | \n4–13.8 | \n[39] | \n
Orange peel | \nAlcohol precipitation | \n7.9 | \n[39] | \n
Aqueous acid extraction alcohol precipitation | \n4.53 | \n[40] | \n|
Cocoa peel | \nMicrowave assisted | \n42.3 | \n[41] | \n
Apple Pomace | \nAcid extraction | \n12.9–20.9 | \n[27] | \n
Lime-peel and pulp | \nMicrowave assisted extraction under pressure | \n8–17.9 | \n[42] | \n
Watermelon rind | \nAcid and enzymatic extraction | \n\n | [43] | \n
Orange peels | \nAcid extraction | \n5.4–26.3 | \n[44] | \n
Sweet potato peels | \nAcid extraction | \n2.59–5.08 | \n[45] | \n
Orange peel | \nUltrasound assisted | \n20.92 | \n[46] | \n
Orange peels ( | \nAcid extraction | \n29.41 | \n[47] | \n
Kaffir lime peel ( | \nChemical and acid extraction | \n61.8 | \n[48] | \n
Acid extraction | \n27 | \n[49] | \n|
Orange peel ( | \nAcid extraction | \n45.5 | \n[50] | \n
Lemon ( | \nAcid extraction | \n2.7–16.7 | \n[51] | \n
Orange ( | \nAcid extraction | \n1.6–15.9 | \n[51] | \n
Grape ( | \nAcid extraction | \n2.3–15.7 | \n[51] | \n
Orange peel | \nWater-based extraction | \n2.2 | \n[52] | \n
Sweet potato peel ( | \nAlkaline extraction | \n16.78 | \n[45] | \n
Tomato waste | \nUltrasound assisted | \n15.1–35.7 | \n[53] | \n
Pumpkin peels | \nSoxhlet extraction | \n6.8–7.7 | \n[54] | \n
Lemon pomace | \nAcid extraction | \n10.3–13.1 | \n[55] | \n
Jackfruit waste ( | \nAcid and chemical extraction | \n12–15 | \n[27] | \n
Lemon peel wastes | \nAqueous extraction | \n\n | [56] | \n
Citric waste | \nAcid extraction | \n78 | \n[57] | \n
Apple peel waste ( | \nAcid and chemical extraction | \n1.21 | \n[58] | \n
Horse eye bean peel ( | \nAcid extraction | \n4.4 | \n[59] | \n
Banana peel | \nAcid extraction | \n11.31 | \n[60] | \n
Mango peel | \nAcid extraction | \n18.5 | \n[60] | \n
Grapefruit peel | \nAlcohol extraction | \n25 | \n[33] | \n
Saba banana peel ( | \nAcid extraction | \n17.05 | \n[61] | \n
Passion fruit peels | \nAcid extraction | \n2.25–14.6 | \n[62] | \n
Citrus peel | \nAcid extraction | \n25.5 | \n[63] | \n
Pumpkin waste ( | \nAcid hydrolysis | \n2.90 | \n[39] | \n
Mango peel | \nAcid extraction | \n20.8 | \n[64] | \n
Jackfruit wastes ( | \nOptimised acid extraction | \n38.42 | \n[65] | \n
Acid extraction | \n4.1 | \n[66] | \n|
Orange peel | \nAcid extraction | \n7.3–52.9 | \n[67] | \n
Jackfruit waste ( | \nChemical and acid extraction | \n8.9–15.1 | \n[27] | \n
Methods of extraction of pectin from various agrowaste compounds.
Large amounts of fruit wastes that are being generated can be disposed effectively by manufacturing beneficial by-products like pectin. Pectin is used to increase foaming power of gases, as agglutinator, as filler in pharmaceutical preparations and also in food industry. The use of pectin for different purposes depends on its characters like acetyl value, degree of esterification, uronic acid content and methoxyl content, etc. [68]. The amount of anhydrouronic acid gives the purity of pectin which is not less than 65% for pectin that is used commercially [69].
\nColour reader can be used to measure the colour of extracted pectin by placing lens of reader on sample powder. The colour of the extracted samples can be compared with that of commercial pectin. Solubility of pectin in different solvents is measured i.e., solubility in cold and, hot water and alkali like NaOH.
\nAcetyl content and equivalent weight of pectin can be estimated using NaOH whereas methoxyl content can be estimated by saponification and titration. Degree of esterification can be calculated from methoxyl content and anhydrouronic acid content. After acid hydrolysis, sugar separation can be achieved by thin layer chromatography. Intrinsic viscosity of pectin is measured by dissolving pectin in water and by preparation of solutions of various concentrations [27, 32, 60].
\nPectin being a great inert, biodegradable and biocompatible complex, is widely used in various fields such as in textiles, food industries as gelling agents, pharmaceuticals and other products as well [70]. Pectin are used as biomaterials in gene delivery [71], application in oral drug delivery [72], as edible coating for food packaging [25], biomass yield and bio refinery [21, 22]. It also has applications in tissue engineering as scaffolds [73], in paper and textile industries for the preparation of ultracentrifugation membrane [74].
\nFrom the very early period of time, pectin had become one of the major natural constituents of human food, and they have been widely used as a gelling agent for jams and jellies. In jam processing, fruits are cooked properly in order to release juice and pectin which converts the proto-pectin into soluble pectin [19]. Pectins are also used as a substitute of sugar in jams that are made without sugar, using LM (low methoxy) pectin due to its stability in acidic condition. Pectin is widely used for making instant jellies for bakery production these are made with the use of HM (high methoxy) pectin that are thermally stable, the only difference between HM and LM pectin is the amount of pectin in the formula, LM requires a higher amount than that of HM [75]. Other food products like artificial cherries [15], are used to make different kinds of gel puddings that is made of pectin present in the fruit syrup and cold milk [25]. Edible coating of food material is also made of pectin [25]. Pectin is used in beverages as a beverage clouding agent like in diabetic soft drinks [76]. Pectins are also used in the fruit preparation of yogurt to make it more soft and to obtain the partial gel texture [77].
\nThe blending of the natural and synthetic polymers is one of the promising areas of development, this gives new polymeric material with better durability and resistance. Materials like sponge, hydrogels, encapsulating drugs etc. are produced by polymer films [32]. Due to development and discovery of natural polymers scientist have started to form bio-based material rather than synthetic one due to its physiochemical properties like biodegradability, this shift is mainly caused due to the environmental issues and concern regarding the heavy use of plastic [78]. Films of pectin are used to encapsulate and thicken food, and in pharmaceuticals [29]. Hoagland et al. made pectin films with glycerol and lactic acid to prevent fungal contamination on the laminated films [47]. The similar kind of products were made by Fisherman et al., where an edible pectin blend film were plasticized with glycerol, they also suggested that the glass transition at about 50°C was large in case of pectin films, which indicates that the films were fairly flexible at room temperature [79]. Liu et al., made different varieties of biofilms one each with pectin, fish skin gelatin and soybean flour protein which in turn resulted in a composite film that showed an increase in stiffness as well as the strength, whereas decrease in water solubility and water vapour transmission rate when compared to the film that was made with pectin alone. They thus suggested that the tensile strength can be improved by crosslinking the films with methanol or glutaraldehyde [80]. A bio-reactive substance for tissue regeneration was developed by Liu et al., which was composed of pectin or PGLA matrix, which demonstrated that pectin was able to carry signals to molecules, further they suggested that the pectin also helped in the adhesion of the cell and promotes cell proliferation [35]. Some researches have reported the use of pectin membranes as a wound dressing material [81].
\nIn recent years, biomedical application especially in case of drug delivery system, the use of natural polymers is preferred over the other types due to their inert nature and its biocompatibility. Pectin as the natural polymer is a new developed interest for drug delivery application due to its properties of gel formation in acidic condition, its mucoadhesiveness and its ability to dissolve in basic environment [36]. These properties of pectin are applied in different ways such as the mucoadhesiveness helps in targeting and controlling the drug delivery especially in the nasal and gastric environment, where as its ability to dissolve in basic condition helps in the release of colon related drugs and the formation of gel helps in increasing the contact time of drug in gastric condition [35, 36]. Recent studies have shown the use of LM pectin for nasal drug delivery due to its mucoadhesive property they have a tendency to bind to the mucin with the help of hydrogen bond [82]. Its use in the production of fentanyl (painkiller) has also been seen that help in treating cancer pain which needs rapid drug release [83, 84]. An alternative for smoking cessation are the nasal pectin containing nicotine [85]. As pectin have resistance towards proteases and amylases it has been highly preferred as an encapsulating nanoparticle for drug delivery as most of the proteins are easily degraded by our digestive enzymes and thus to protect these drugs the use of pectin as an outer cover that cannot be degraded in the gastrointestinal tract are preferred for colon and oral drugs [86]. Studies have shown that pectin is able to inhibit cancer metastasis and primary tumour growth in many animal related cancer [87, 88]. Gal-3 is one of the important factors controlling cancer progression and metastasis, and pectin has the ability to recognise these Gal3 components [89]. In a study, citrus pectin was used to target Gal3 that could inhibit the metastatic successfully [87, 90].
\nThe treatment of any genetic disorder is called gene therapy as it deals with the defected genes that are responsible for the disorder; these are treated by replacing the defective gene, silencing the unwanted gene expression or by substituting missing genes and these are carried out with the help of viral or non-viral vectors [36]. The use of non-viral vectors is preferred over viral due many reasons like biocompatibility, minimal toxicity and immunogenic reactions of our body [71]. These non-viral vectors are made of polymers of polycationic, chitosan or even pectin. It has been observed that the use of carbohydrate mediated products have better binding capacity, to facilitate the uptake by target cell [91, 92, 93]. Pectins were found to be suitable as a coating substance for b-PEI [94, 95]. Opanasopit et al. has also observed the formation of pectin nanoparticle which in turn helps to entrap the DNA for transfection [96]. Katav et al., modified pectin with the help of three different amine groups and these complexes were able to bind with plasmid DNA and there efficiency to transfect or their potential as a non-viral gene delivery carrier was compared and suggested that modified pectin has a promising role in gene delivery [71]. Similar type of study was conducted by Opanaopit et al., where pectin ability as a nanoparticle for gene delivery were studied and the study suggested the potential use of pectin as delivery vector to be safe [96]. Pectin has also been used as wound dressing material in the form of pectin-chitosan based nanoparticles. It has the ability to create an acidic environment in which the bacteria cannot grow. Burapapadh et al. developed a pectin based nanoparticle to improve and enhance the drug dissolution of ITZ (Itraconazole) [97].
\nScaffolds are 3-D biomaterials that are porous in nature and are designed to be applied in various fields, few of its basic functions are to promote cell adhesion, to allow enough nutrients and gases transportation and mainly for tissue engineering [32]. Tissue engineering mainly involves the use of biocompatible scaffolds materials to act as a support matrix or to be used as a substrate for delivery of some compounds. There has been a great research going on to promote tissue reconstructions. Coimbra et al., prepared pectin based scaffolds to be used for bone tissue engineering [98]. Similar study was performed by Munarin et al., who examined the use of pectin as injectable biomaterial for bone tissue engineering [99]. Ninan et al. were also able to fabricate biopolymer scaffold of pectin and other compounds using the technique of lyophilisation, thus suggested the use of pectin as ideal polymeric matrix for tissue engineering [73, 100, 101].
\nPectin is one of the most extensively studied natural biodegradable polymer. In spite of its availability in a large number of plant species, commercial sources of pectin are very limited. There is, therefore, a need to explore other sources of pectin or modify the existing sources to obtain pectin of desired quality attributes. Current knowledge of the molecular basis of pectin has helped us to understand some aspects of this complex polysaccharide. Extensive studies must be carried out to find out more about the biological pathways to devise various efficient means of pectin extraction that are scalable and can be commercialized. The large variety of applications as well as the increasing number of studies on pectin suggests that the potential of pectin as novel and versatile biomaterial will be even more significant in the future. As the research and development continues in pectin-based products, we expect to see many innovative and exciting applications.
\nThe authors would like to thank Fr. Jobi, Head of the Department of Life Sciences, for providing laboratory facilities and supporting this work.
\nThe authors would like to declare that there was no conflict of interest in this work.
\nA regulated diet with all the constituents consumed in appropriate way maintains cell homeostasis and keeps the body under physiological state that are essential for cellular demands. A number of factor contribute to body function such as biomolecules, vitamins, minerals, and hormones etc.….of these minerals gain utmost importance due to availability inside the cell is low but shows a major effects even small change in concentration. Minerals perform wide variety of functions, which are essential for existence of organism. Some of them form integral components, some as cofactors, and some as essential components of enzymes. The existence of these minerals as part of enzymes helps to play a role in metabolism of molecules consumed through diet and maintain cell homeostasis. Some of the minerals acts in concert with aid of hormones according to their need in specific organelle. Minerals either in part or in combination with vitamins shows major functions required for the cell and their deficiencies shows adverse side effects although not hereditary. Minerals classified according to the need includes major (phosphorous (P), potassium (K), calcium (Ca), magnesium (Mg), sulphur (S)), minor/trace/rare (Boron (B), chlorine (Cl), chromium (Cr), fluoride (F), iodine (I), iron (Fe), manganese (Mn), molybdenum (Mo), nickel (Ni), selenium (Se), sodium (Na), vanadium (V) and zinc (Zn)). In this chapter a detailed explanation of selected minerals about their importance as a source requirement, uptake and transport mechanism, toxicity and tolerance mechanism, taken as means of measurement for determining their beneficial effects to study in detail about the specific role in metabolism their mechanism of action and deficiency diseases associated with reduced life span had described.
\nDecline of physiological functions leading to senescence of cells with arrest at G1 phase is characteristic feature of ageing [1]. At cellular level senescence was caused due to several factors such as oxidative stress, mitochondrial dysfunction, inflammation, autophagy deregulation, telomere shortening [2, 3]. Cells senesce either due to continuous replication or due to stress induction thereby activating p16, p53 pathways and phosphorylation of Rb protein [4] leading to inflammatory condition with high lysosomal β-galactosidase activity [5, 6, 7]. As cells continuously, divide chromosomes containing telomere with repeated nucleotides region gets shortened [8] leads to replicative senescence [9] and result in ageing. In humans, the repeated sequence at telomere region is TTAGGG [10]. Cells capable of replicating continuously express telomerase for replication of telomere ends of chromosome, which had tendency to reverse ageing process and used as targeted approach [2]. Increased ROS production due to stress apart from normal cellular homeostasis as a compensatory mechanism aggravates ageing phenomenon. Free-radical theory proposes ROS leads to oxidative damage and contributes to plays a role in the ageing process [11]. First call to increased ROS levels inside the cells is activation of survival pathways, which further leads to apoptosis due to failure of antioxidant system to defence against ROS that ultimately leads to cell death [12, 13]. Several factors were responsible for production of ROS that disturbs balance between cell survival and cell death through increased redox potential towards pro-inflammatory state and connects oxidative stress, inflammation and ageing [14, 15, 16]. The release of pro-inflammatory agents inside the senescent cells include TNF-α, IL-6, IL-1β [17] regulated by transcription factors such as AP-1, NFκB [18]. The activation of AP-1, NFκB requires kinases such as ERK, JNK, p38MAPK, PI3K [19] and leads to expression of target proteins such as MMP9, ICAM-1, iNOS, COX-2 [20, 21, 22]. Mitochondria apart from playing a role in oxidative phosphorylation system it also plays a role in apoptosis, metabolism, innate immunity and ageing [23, 24, 25]. Mitochondrial regulation occurs through PGC-1 (α & β) that responds to NAD+ levels inside the cell [26, 27] and in response to SIRT1 regulation occurs by HIF-1α independent of PGC-1 [28]. In ageing NAD+ levels decreases without loss of SIRT1 but downregulates it [29]. One of the contributing factor for cell survival under stress conditions is autophagy [30]. Autophagy is downregulated under nutrient rich conditions through mTOR protein [31] and stimulated through AMPK by phosphorylating mTOR (inactivation) ultimately activating ULK-1 [32]. Reports reveal autophagy deregulates due to overexpression of mTOR [33, 34] in ageing. Several Genetic events (mTOR, TGFβ), Molecular events (oxidative stress, autophagy) also contribute to ageing phenomenon. A summary of factors responsible for cellular ageing were shown in Figure 1.
\nFactors responsible for aging: Different factors enhances process of aging includes autophagy, oxidative stress, shortening of telomere, caloric restriction, proteostasis, inflammation, mitochondrial dysfunction and DNA damage.
Phosphorous is mostly present in meat, fish, eggs, and milk and dietary intake is 0.8-1.0 g/day. Phosphorus is essential for the formation of healthy bones, part of buffer system and component of DNA and RNA. Functions of phosphorous include formation of high-energy phosphates, nucleic acids, nucleotide coenzymes. Activation of enzymes require phosphate moiety and found in cell walls. Phosphorus deficiency include rickets, osteomalacia observed mostly in cases of malnutrition, anorexic individuals, or alcoholics. Symptoms are poor appetite, anxiety, and irritability. Phosphate absorption occurs in jejunum calcitriol, low pH favours their absorption while phytate reduces its absorption. Serum phosphate level is about 3-4 mg/dl and reduced in renal rickets, vitamin D deficient rickets and in diabetes mellitus. Phosphate excreted by kidney in the form of urine. Phosphate is mainly involved in mineralisation of the bone from chondrocytes and osteoblast. The process of mineralisation begins with hydroxyapatite formation from calcium (Ca + 2) and inorganic phosphate. Calcium incorporated through annexin calcium channel here as inorganic phosphate from type III sodium inorganic phosphate transporter and from PHOSPHO1. Hydroxyapatite penetrate the matrix vesicle and elongate due to tissue non-specific alkaline phosphatase (TNAP) and deposit in collagen fibre spaces [35]. The role of phosphorous in bone mineralisation shown in Figure 2a. Osteomalacia resulting from hypophosphatemia occurs through fibroblast growth factor signalling (FGF) [36] that links with ageing process [37]. Reduced phosphate levels inside the cell leads to increased FGF 23 levels in the serum and acts by inhibiting calcitriol, PTH, 1α-hydroxylase and stimulating 24-hydroxylase [38]. The signalling pathway connecting phosphorous deficiency and ageing shown in Figure 3.
\nRole of mineral elements in disease prevention. a: Role of phosphorous in bone mineralisation, b: Potassium involvement in muscle contraction, c: Calcium in bone calcification, d: Magnesium in protection of neuron degeneration, e: Sulphur in prevention of muscle pains and joint pains, f: Fluorine in preventation of dental caries, g: Iodine in thyroid hormones, h: Iron in haemoglobin synthesis, i: Sodium in heart function, j: Zinc in immunity.
Deficiency disease leads to aging through disturbed signalling pathway. Mineral deficiencies were shown in parenthesis. Ca: Calcium, I: Iodine, Mg: Magnesium, P: Phosphorous, Na: Sodium, S: Sulphur, Zn: Zinc, F: Fluorine, K: potassium, Fe: Iron. TSH: Thyroid stimulating hormone, Nrf 2-nucleoid erythroid receptor factor 2. FGF-fibroblast growth factor, SIRT1; Sirtuins 1, mTORC1: mammalian target of rapamycin complex 1, NFκB: Natural factor kappa beta, IL-6: interleukin 6, TGF-tumor growth factor, MAPK-mitogen activated protein kinase, Wnt-Wingless-related integration site.
Potassium is principal intracellular cation required daily about 3-4 g that is present majorly in banana, orange, potato, chicken, and liver. It helps regulate fluid balance, nerve signals and muscle contractions and beneficial aspects include reduction in blood pressure, water retention; prevention of kidney stones, osteoporosis, and protection against strokes. It functions to maintain intracellular osmotic balance, regulation of acid–base balance, required for transmission of nerve impulse, and necessary for biosynthesis of proteins. Plasma levels are 3.4-5 mEq/L absorbed through intestine excreted in form of urine. Deficiency diseases include muscle weakness, mental confusion. Potassium ion present on the cells as potassium ion channels and various types of potassium ion channels include ATP-sensitive K channels (KATP), voltage-dependent K channels (Kv), Ca2+ − and voltage-dependent K channels (BKCa), inward rectifier K channels (Kir), and tandem two-pore K channels (K2P) their activity varies in different types of diseases [39]. Potassium as known to play a role in Na + -K+ ATPase for effective muscle contraction [40] and motor regulation is by ATP driven potassium channels [41]. ATP driven potassium channel deficiency affected resting tension of skeletal muscle [42] deficiency of potassium ions alters sodium potassium pump of skeletal muscle and augments its contraction in ageing [43]. According to previous reports, high potassium levels depolarizes smooth muscle cells that opens up voltage gated calcium channels resulting in entry of calcium ions inside the cells thereby leading to activation of smooth muscle contraction [44] The role of potassium in muscle contraction shown in Figure 2b. It had reported that activation of mTORC1 signalling correlated with decline in muscle mass [45, 46] activated mTORC1induces oxidative stress that leads to protein degradation, autophagy and necrosis showing an aged phenotype [47]. The signalling pathway connecting potassium deficiency and ageing shown in Figure 3.
\nBiological availability of calcium is green leafy vegetables, nuts, seafood, cereals etc. Cow’s milk is rich source of calcium and required daily about 0.8-1.0 g/day. Calcium plays an important role in development of bones, muscle contraction, blood coagulation, nerve transmission, membrane integrity, activation of enzymes, intracellular messenger, contact inhibition, nerve excitability, skeletal muscle integrity and maintenance, and cardiac tone. Factors promoting calcium absorption include low pH, parathyroid hormone, vitamin D, lactose. Most of blood calcium is in plasma and ranges about 9-11 mg/dl. Factors regulating plasma calcium include calcitriol, parathyroid hormone, and calcitonin. Calcium excreted mostly through intestine and partly by kidneys. Deficiency of calcium leads to hypocalcemia and shown signs such as fragility of bone, muscle cramping, and dry skin. Deficiency diseases include rickets osteomalacia, osteoporosis. Evidences reveal that calcium is involved in bone calcification where osteoblasts secrete collagen as ground substance and polymerises it then osteoblast entrap osteoid and calcium salts precipitates as non-crystalline amorphous substance. Reabsorption and reprecipitation of hydroxyapatite crystals makes bone calcified. Existing reports evidence that stimulation of PGC-1α signalling regulate osteoporosis and ageing [48]. The role of calcium in osteoblast calcification shown in Figure 2c. Recent reports reveal that Wnt, MAPK, oestrogen pathways are targets for osteoporosis and ageing, it had shown that Wnt pathway responsible for production of sclerotin is dysregulated and MAPK pathway altered in osteoporosis [49]. The signalling pathway connecting calcium deficiency and ageing shown in Figure 3.
\nSources of this mineral include milk, meat, fruits, and cereals. Biochemical functions include formation of bone, teeth, neuromuscular irritability, and cofactor for enzymes (kinases). Daily intake is 300-350 mg, serum concentration is 2-3 mg/dl and deficiency leads to convulsions, neuromuscular irritation, uraemia, and rickets. Magnesium absorption occurs in intestine alcohol inhibits it whereas parathormone enhances it. Causes of magnesium deficiency include alcohol abuse, poorly controlled diabetes, excessive or chronic vomiting and/or diarrhoea. Research on neurodegenerative diseases reveal magnesium had neuroprotective role by inhibiting influx of amyloid β from blood and promote its clearance [50] furthermore it attenuates impairment in long-term potentiation and impaired recruitment of synaptic proteins through activation of PI3K/Akt and inhibition of GSK3 β thereby reducing neuronal damage [51]. To date several reports indicate that Nrf-2 an antioxidant responsive protein plays a role in protection of cells from oxidative stress and essential for optimal activity inside the cell [52]. The role of magnesium in neuro degeneration shown in Figure 2d. Dysregulated Nrf-2 activity in neurodegenerative diseases linked to ageing [53, 54]. The signalling pathway connecting magnesium deficiency and ageing shown in Figure 3.
\n2.5 Sulphur (S): Egg white, chicken, fish, beef are major sources of sulphur. Daily intake is 14 mg for healthy adult and distributed in nails, hair, and skin. Sulphur plays a role as antioxidant, anti-inflammation, metal transport, free radical scavenging, protein stabilisation, xenobiotic detoxification, metabolism of lipids. Sulphur resides inside the body in organic form as methionine, cysteine, and cysteine functions as part of vitamins such as thiamine, biotin, and coenzyme A and excreted through oxidised form as taurine and cholic acid. Deficiency diseases are almost unknown. Although reports revealed that, sulphur containing amino acids in the form of methionine and cysteine forms creatinine, carnitine and coenzyme. Sulphur in the form of methylsulfonylmethane (MSM) acts to prevent muscle pains and joint pains through reduction of pro-inflammatory cytokines (NFkB, IL-1, IL-6, IL-8, TNF-α) [55, 56, 57] and decreased infiltration of immune cells by reducing inflamed synovial membrane [58, 59]. The role of sulphur in muscle pains and joint pains shown in Figure 2e. An essential for muscle functioning and deficiency leads to muscle impairment and aged phenotype. Aged muscle has altered Redox signalling [60, 61, 62] and exercised individuals in their lifetime had preserved enough muscle fitness comparable to younger ones [63] whereas NAD+ treatment [28] reverse these effects. Strenuous exercise result in muscle damage [64] and dysregulated redox response within the muscle increase in transient ROS/RNS. This clearly explains redox mechanisms operate with ageing and contraction of skeletal muscle can activate a number of transcription factors thereby affecting gene expression of specific cellular pathways. The signalling pathway connecting sulphur deficiency and ageing shown in Figure 3.
\nIt occurs mostly in soil and water; dietary sources include leafy vegetables, pineapple, dry fruits, lemon, nuts, and berries and daily intake is <20 mg. It is ingested through diet and found higher quantities in hair, nails, bone whereas fat tissue being low [65]. It is absorbed into the intestine through boric acid and stored in tissues. The toxic effects of boron include DNA damage and repair and has effect on protein folding and stability. In infants, excess of boron leads to anaemia, seizures, erythema, dermatitis, cardiac problems [66, 67, 68]. Chronic exposure leads to disorders of brain, kidney, and testis (88). Boron determination utilises spectrophotometry [69], spectrofluorimetry [70], potentiometry [71], inductive coupled plasma atomic emission spectroscopy [72], and inductive coupled plasma mass spectrometry techniques [73]. Beneficial effects include reduction in sterility, osteoporosis, inflammation, coagulation, and cancer. Its application widely relays on food and medicinal sector.
\nFluoride levels abundantly found in barley, rice, cassava, canned fruits and least in food grain, breast milk, beverages and daily intake is about 2 ppm. Fluoride levels in the environment is taken up either by food, water or inhaled by air, drugs and reach the digestive tract for metabolism and distributed inside the body bone, soft tissue, milk, tooth. The factors that influence the fluoride metabolism inside the body include acid–base disorders, hormones, physical activity, cardiac rhythm, and diet. Fluorine functions as prevention of dental caries, necessary for development of bones. The mechanism of action of fluoride inside the body involves inhibition of demineralisation of enamel. A small amount may substantially contribute to health benefits that include dental caries, decreases acid production. High levels leads to alterations in cell architecture, abnormalities in hepatic and renal systems. Fluoride poisoning inside the cells diagnosed by contraction of muscle, stiffness of body, failure of respiratory and cardiac systems. The methods for removing excess of fluorine done using coagulation-precipitation, electro coagulation, adsorption etc. Excreted through faeces, urine. Deficiency diseases include dental caries, osteoporosis. Fluoride helps in remineralisation, crystallisation and Fluoroapatite formation through enhancement of tooth and improves against acid resistance thereby preventing dental caries [74]. The role of fluorine in dental caries shown in Figure 2f. Reports reveal that klotho/KLF4 protein is involved in secretion of saliva from salivary gland and attenuation of KLF4 pathway thereby inactivating mTOR, AMPK, cyclin D1 that leads to dental caries [75]. The signalling pathway connecting fluoride deficiency and ageing shown in Figure 3.
\nIt is abundant in seafood, iodised salt and daily intake is about 150-200 ug. It is component of thyroid hormones stored in the form of thyroglobulin and toxicity symptoms include thyrotoxicosis, goitre. Iodine is mainly absorbed through small intestine but also occurs through skin and lungs. Plasma level is 4-10 mg/dl. Iodine mainly excreted through kidney but also through skin, milk saliva and bile. Deficiency causes cretinism, goitre, and myxoedema. It is evident from existing reports that iodine uptake by thyroid cells occurs with the help of sodium iodine symporter and translocates to apical membrane fuses with thyroglobulin with the help of thyroperoxidase to form monoiododthyronine (MIT), diiodothyronine (DIT) in thyroid follicle cells. Coupling of MIT & DIT results in triiodothyronine (T3) & tetra iodothyronine (T4) which is internalised through endocytosis that releases free T3, T4 into the blood stream. Iodine deficiency leads to uptake of more thyroid-stimulating hormone (TSH) into thyroid cells for production of thyroid hormones (T3 & T4) which results in enlargement of thyroid gland to form goitre [76]. Age associated abnormality of thyroid gland is not consequence of ageing but result of thyroid autoantibodies that leads to age associated diseases [77]. The role of iodine in goitre shown in Figure 2g. Disturbed TSH signalling found in ageing individuals due to reduced release of TRH and less production of TSH thereby lowering the thyroid gland response to TSH with concomitant release of T3 and T4 [78] and enhances Ras activity that leads to increase of thyroid gland cell proliferation [79]. The signalling pathway connecting iodine deficiency and ageing shown in Figure 3.
\nIron (non-heme) abundantly found in cereals, pulses, fruits, vegetables whereas heme is from poultry, fish and daily requirement is about 10-15 mg. Iron present in the form of heme transports oxygen, involved in electron transport chain, required for phagocytosis in form of peroxidase. Iron is absorbed in stomach and duodenum low pH, vitamin C enhances its absorption whereas phytate and oxalate interfere its absorption. Enterocytes absorb iron through metal transporter 1 protein and gets metabolised (heme) through heme oxygenase-1 [80, 81]. Inhibitors of iron absorption includes phytic acid [82], polyphenols [83], and calcium [84] whereas ascorbic acid is enhancer [85]. Iron is transported inside the body through circulating proteins namely transferrin, lactoferrin, ferritin, heme proteins [86]. Iron regulation inside the cells occurs by 2 mechanisms one is by binding of iron responsive elements (IRE) [87] to iron responsive proteins (IRP) and other by Hepcidin. Gene mutations of transferrin receptor 2, haemochromatosis, haemochromatosis type 2, hepcidin antimicrobial peptide (HAMP) [88] for impaired expression had observed. Iron storage inside the body is by ferritin [89] in liver, spleen, bone marrow [90]. Bodily iron is mostly excreted in form of blood through menstrual release and other forms includes skin and gastro intestinal tract [91] but not through urine. Iron deficiency results in depletion of iron and primary cause is low bioavailability of iron. It also occurs through pregnancy, menstruation, and pathologic conditions [92, 93]. Anaemia is the sign of iron deficiency [94]. Iron deficiency overcome by improvement in iron uptake and bioavailability, supplementation of iron with food and its fortification. Deficiency diseases include hypochromic microcytic anaemia. Reports evidence that iron (Fe+2) is absorbed by duodenal cells and binds with apoferritin to form ferritin which then binds to heme carrier protein (HCP) to form ferroportion (FPN). Ferroprotein is either stored in liver or transported in the blood, combines with transferrin in blood and reach erythrocytes that then binds to transferrin receptor and internalised into the cell and gets dissociated with the help of divalent metal carrier transporter 1 and performs functions such as erythropoiesis, cell metabolism, myoglobin production in muscles. Heme combines with myoglobin to form haemoglobin [59]. Recent reports reveal that PR domain zinc finger protein 8 (PRDM8) gene had a role in premature ageing of haematopoietic cells through DNA methylation that leads from aplastic anaemia (AA) patients independent of telomere attrition a haemoglobin disorder [95]. The role of iron in haemoglobin synthesis shown in Figure 2h. Reports also state that anaemia resulting from erythropoiesis of haematopoietic ageing of intrinsic altered microenvironment had upregulated IL-6, TGF-β signalling [96]. The signalling pathway connecting iron deficiency and ageing shown in Figure 3.
\nThe daily intake of molybdenum was 75-250 ug and toxicity characterised by gout and joint pains. Molybdenum is present as cofactor for nitrate reductase, Xanthine oxidase and sulphite oxidase enzymes. Molybdenum cofactor biosynthesis occurs in steps formation of precursor Z from GTP, synthesis of molybbdeoprotein from precursor Z, addition of adenyl group to molybdoprotein and its insertion [97]. Molybdenum uptake inside the cells occurs with the help of ATP binding cassette transporters [98]. Molybdenum deficiency results in improper functioning of enzymes responsible for specific metabolic pathways in which they were involved and leads to metabolic diseases such as Xanthinuria, Hyperuricemia, and neurodegeneration. Deficiency diseases are almost unknown but some reports reveal its deficiency leads to chrons disease.
\nAbundantly found in common salt and other sources include leafy vegetables, milk, eggs, and nuts and daily intake is about 5-10 g. Absorbed as sodium ions and circulates inside the body in plasma and plasma levels were 135-145 mEq/L. It is cheif extra cellular cation regulates acid–base balance and involved in osmotic pressure. It is involved in activation & transmission of nerve impulse, absorption of biomolecules and aldosterone. High levels were observed in cushions disease and low levels were observed in addisons disease. Excreted from kidney in the form of sodium chloride through urine or as phosphate and other routes is by sweat. Deficiency diseases are almost unknown but reports reveal that higher risk of cardiovascular disease with low sodium intake [99]. Sodium inside the cells were present as sodium channels as (sodium-potassium ATPase, sodium-proton antiporter) the role of sodium in heart function is mostly presented by stimuation of aldosterone which enhaces its influx into the cell and activates inositol 1,4,5 tri phosphate (IP3) [100, 101]. Activated IP3 releases stored calcium from endoplasmic reticulum and makes excitation coupled to contraction for effective heart function [102]. The role of sodium in heart function shown in Figure 2i. SIRT1, mTORC1 regulate cell balance between cell growth and survival. Activation of SIRT1 along with PGC-1α, AMPK and inhibition of mTORC1 along with Akt act to prolong cell longevity and retard cardiac ageing. Autophagy underlies the activation of SIRT1/PGC-1 α/AMPK and inhibition of Akt/mTORC1 responsible for cardiac ageing. Chronic heart failure involves deficient autophagy phenomenon through hyperactivation of Akt/mTORC1 and suppression of SIRT1/PGC-1 α/AMPK pathway that finally leads to cardiac ageing [103, 104]. The signalling pathway connecting sodium deficiency and ageing shown in Figure 3.
\nZinc mostly found in meat, cabbage, dates, mushrooms etc. and daily intake is 10-15 mg. Exposure of zinc is mainly by three ways inhalation, dermal exposure, oral exposure [105] and excess zinc shows symptoms such as abdominal pain, nausea, anaemia, gastrointestinal effects. Zinc plays an essential role as structural, catalytic, mild deficiency causes oligospermia, hyperammonemia [106]. Zinc is absorbed in duodenum phytate inhibits absorption whereas amino acids enhances its absorption. Oral uptake of zinc absorbs through small intestine and distributed in serum by binding to albumin, α-microglobulin, and transferrin [107]. Zinc homeostasis occurs mainly with the help of transport proteins namely Zinc importer (ZIP) and zinc transporter (ZnT) [108] which then binds to metallothionin, and sequester to other cell organelle. Beneficial aspects of zinc were antioxidant [109], antidepressant, antidiabetic [110], delayed wound healing, and anticancer [111]. Toxic effects of zinc observed when it crosses more than 100-300 mg/day typical symptoms include reduction of HDL and cholesterol levels, vomiting, lethargy, and fatigue. Serum zinc levels is about 100 mg/dl. Excretion of zinc occurs mainly by kidney, skin, and intestine. The role of zinc as immune protector well studied as anti-inflammatory and performs its action through reducing intracellular ROS by activating superoxide dismutase (SOD), NADPH oxidoreductase (NOX), metallothionin (MT) thereby suppressing inflammatory pathway (NFkB) and reduces it [112]. The role of zinc in immunity shown in Figure 2j. Zinc deficiency induces oxidative stress activates transcription factors NFkB, AP 1 through NFkB signalling in ageing process [113, 114]. The signalling pathway connecting zinc deficiency and ageing shown in Figure 3.
\nMinerals play an important role in daily life ranging from nuts to leafy vegetables. Minerals mainly function as cofactors along with enzymes to show their metabolic effect. Minerals form holoenzymes in metabolism of biomolecules and help in cellular vital process for cell survival. In their absence, the show some deficient metabolic effects and required in small amounts to function effectively. Intake varies from infants to adults, gender excess amounts shows hyper forms, and low amounts leads to hypo effects. Mineral deficiencies mostly show aged phenotype and age related diseases have mineral deficiencies. In their absence cell, survival pathways are mostly non-functional and leads to decreased metabolic function that is characterised by aged phenotype. Minerals classified mostly upon their requirement as major (phosphorous (P), potassium (K), calcium (Ca), magnesium (Mg), sulphur (S)), minor/trace/rare (Boron (B), chlorine (Cl), chromium (Cr), fluoride (F), iodine (I), iron (Fe), manganese (Mn), molybdenum (Mo), nickel (Ni), selenium (Se), sodium (Na), vanadium (V) and zinc (Zn)). A selected mineral with their function importance in mammals have been described in detail in which Phosphorous (P), Potassium (K), Calcium (Ca), Magnesium (Mg), Sulphur (S), Fluoride (F−), Iodide (I−), Iron (Fe), Sodium (Na), Zinc (Zn) along with mechanism of action and its diseased mechanism associated with ageing. Phosphorous is involved in bone mineralisation from osteocyte through hydroxyl apatite formation and deficiency leads to osteomalacia that related to ageing through increased fibroblast growth factor signalling. Potassium is involved in muscle contraction and its deficiency leads to muscle weakness and shows aged phenotype through enhanced mTORC1 signalling. Calcium is involved in bone calcification through hydroxyl apatite crystals its deficiency leads to bone disorders shows aged phenotype through dysregulated Wnt, MAPK pathway. Magnesium is involved in protection of neuron from degeneration through inhibition of GSK3β signalling and hyper activation of PI3K, Akt signalling and shows aged phenotype through dysregulated Nrf 2 pathway. Sulphur is involved in prevention of muscle pains and joint pains by reducing inflammation by scavenging free radicals its deficiency leads to muscle fatigue shows aged phenotype through reduced redox signalling. Fluorine is involved protection of enamel layer by remineralisation, crystallisation of dentine and enhancement in acid resistance its deficiency leads to dental caries which is also an aged phenotype due to disturbed KLF4pathway. Iodine is necessary for thyroid gland for production of thyroid hormones deficiency of it leads to goitre that is characterised by thyroid gland enlargement seen mostly in aged people or people taking iodine deficient diets that occurs through reduced TSH signalling. Iron is necessary for body for haemoglobin synthesis for oxygen transport and its deficiency leads to anaemia an aged phenotype occurs through enhancement in IL-6, TGFβ signalling. Sodium shows its effect by action of aldosterone on muscle cells and helps in heart function deficiency leads to heart diseases an aged phenotype occurs through increased SIRT1, mTORC1 signalling. Zinc well known for immune defence through inhibition of NFκB signalling deficiency leads to reduced immunity through enhancement of this signalling. A summary of different minerals and their mechanism of action along with their associated signalling pathway with ageing had described in Table 1.
\nMineral | \nPhysiological function | \nMechanism of action | \nDeficiency disease | \nSignalling pathway associated with ageing | \n
---|---|---|---|---|
Phosphorous (P) | \nFormation of high energy phosphates, nucleic acids, nucleotide coenzymes | \nBone mineralisation through hydroxyapatite formation [35] | \nOsteomalacia | \nFGF signalling [36, 37] | \n
Potassium (K) | \nChief cation of intracellular fluid, osmotic balance, muscle function | \nContraction of smooth muscle cell [44] | \nMuscle weakness, mental retardation | \nmTORC1 signalling [47] | \n
Calcium (Ca) | \nDevelopment of bones, muscle contraction, blood coagulation, nerve transmission, intracellular messenger etc. | \nBone calcification through formation of hydroxyl apatite crystals | \nRickets, Osteoporosis, Osteopetrosis (marble bone disease) | \nWnt, MAPK pathway [49] | \n
Magnesium (Mg) | \nConstituent of bones, cofactor for kinases | \nProtects neuronal cell death by activating PI3K/Akt signalling [51] | \nNeuromuscular weakness, muscle irritation | \nNrf 2 pathway [53, 54] | \n
Sulphur (S) | \nConstituent of vitamins, heparin, chondroitin sulphate | \nReduces muscle pain and body pain [55, 56, 57] | \nMuscle fatigue, convulsions | \nRedox signalling [60, 61, 62] | \n
Fluorine (F) | \nFormation of bones and teeth | \nPrevents dental caries by remineralisation of enamel and improving acid resistance [74] | \nDental caries | \nKLF 4 pathway [75] | \n
Iodine (I) | \nConstituent of thyroxine, triiodothyronine | \nPrevents thyroid enlargement through T3 &T4 [76] | \nGoitre, Myxoedema | \nTSH signalling [78] | \n
Iron (Fe) | \nTransports oxygen in constituent of heme | \nHaemoglobin formation through erythropoiesis [59] | \nHypochromic microcytic anaemia | \nTGF-β signalling [96] | \n
Sodium (Na) | \nChief cation of extracellular fluid, osmotic balance, acid–base balance, nerve function | \nRegulates heart function through IP3signaling by aldosterone [100, 101, 102] | \nHeart disease | \nSIRT1, mTORC1 signalling [103, 104] | \n
Zinc (Zn) | \nCofactor for alcohol dehydrogenase, carbonic anhydrase, lactate dehydrogenase | \nReduces intracellular ROS by activating SOD, NOX, MT [112] | \nGrowth retardation, hypogonadism, decreased immunity | \nNFkB signalling [113, 114] | \n
Summary of mineral elements mechanism of action and association with longevity.
Abbreviations: FGF-fibroblast growth factor, SOD-superoxide dismutase, NOX-NADPH oxidase, MT-metallothionin, T3-tri iodothyronine, T4-tetra iodothyronine, PI3K-Phosphatidyl inositol 3 kinase, MAPK-mitogen activated protein kinase, Wnt-Wingless-related integration site, Nrf 2-nucleoid erythroid receptor factor 2, TSH-thyroid stimulating hormone, TGF-tumour growth factor, SIRT 1-sirutin1, mTORC1-mammalian target of rapamycin complex 1, NFkB-natural factor kappa beta.
Ca | calcium |
I | iodine |
Mg | magnesium |
P | phosphorous |
Na | sodium |
S | sulphur |
Zn | zinc |
F | Fluorine |
K | potassium |
Fe | iron |
TSH | thyroid stimulating hormone |
Nrf | nucleoid erythroid receptor factor |
FGF | fibroblast growth factor |
SIRT | sirtuins |
mTORC | mammalian target of rapamycin complex |
NFkB | natural factor kappa beta |
IL | interleukin |
TGF | tumour growth factor |
MAPK | mitogen activated protein kinase |
Wnt | Wingless-related integration site |
FGF | fibroblast growth factor |
SOD | superoxide dismutase |
NOX | NADPH oxidase |
MT | metallothionin |
T3 | tri iodothyronine |
T4 | tetra iodothyronine |
PI3K | phosphatidyl inositol 3 kinase |
ZIP | zinc importer |
ZnT | zinc transporter |
GSK3β | glycogen synthase kinase 3β |
ROS | reactive oxygen species |
RNS | reactive nitrogen species |
HDL | high density lipoprotein |
PGC-1α | peroxisome proliferator-activated receptor gamma coactivator 1-alpha\n |
IP3 | inositol 1,4,5 tri phosphate |
ATPase | adenosine tri phosphatase |
GTP | guanosine triphosphate |
PRDM8 | PR domain zinc finger protein 8 |
AA | aplastic anaemia |
HCP | heme carrier protein |
FPN | ferroportion |
IRP | iron responsive proteins |
IRE | iron responsive elements |
HAMP | hepcidin antimicrobial peptide |
MIT | monoiododthyronine |
DIT | diiodothyronine |
TSH | thyroid-stimulating hormone |
AMPK | adenosine monophosphate kinase |
DNA | deoxyribose nucleic acid |
RNA | ribose nucleic acid |
NAD | nicotinamide adenosine dinucleotide |
TNF | tumour necrosis factor |
MSM | methylsulfonylmethane |
FGF | fibroblast growth factor signalling |
PTH | parathormone |
TNAP | tissue non-specific alkaline phosphatase |
ULK 1 | Unc-51 like autophagy activating kinase (ULK1/2) |
MMP | matrix metallo proteinase |
ICAM | inter cellular adhesion molecule |
iNOS | induced nitric oxide synthase |
COX | cyclooxygenase |
RDA | recommended dietary allowance |
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",metaTitle:"Advantages of Publishing with IntechOpen",metaDescription:"We have more than a decade of experience in Open Access publishing. \n\n ",metaKeywords:null,canonicalURL:null,contentRaw:'[{"type":"htmlEditorComponent","content":"We have more than a decade of experience in Open Access publishing. The advantages of publishing with IntechOpen include:
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\n\nOur reputation – Everything we publish goes through a two-stage peer review process. We’re proud to count Nobel laureates among our esteemed authors. We meet European Commission standards for funding, and the research we’ve published has been funded by the Bill and Melinda Gates Foundation and the Wellcome Trust, among others. IntechOpen is a member of all relevant trade associations (including the STM Association and the Association of Learned and Professional Society Publishers) and has a selection of books indexed in Web of Science's Book Citation Index.
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\n\nOur reach – Our books have more than 130 million downloads and more than 146,150 Web of Science citations. We increase citations via indexing in all the major databases, including the Book Citation Index at Web of Science and Google Scholar.
\n\nOur services – The support we offer our authors and editors is second to none. Each book in our program receives the following:
\n\nOur end-to-end publishing service frees our authors and editors to focus on what matters: research. We empower them to shape their fields and connect with the global scientific community.
\n\n"In developing countries until now, advancement in science has been very limited, because insufficient economic resources are dedicated to science and education. These limitations are more marked when the scientists are women. In order to develop science in the poorest countries and decrease the gender gap that exists in scientific fields, Open Access networks like IntechOpen are essential. Free access to scientific research could contribute to ameliorating difficult life conditions and breaking down barriers." Marquidia Pacheco, National Institute for Nuclear Research (ININ), Mexico
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