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Vitamin C Is an Essential Antioxidant That Enhances Survival of Oxidatively Stressed Human Vascular Endothelial Cells in the Presence of a Vast Molar Excess of Glutathione
Cellular glutathione levels may exceed vitamin C levels by 10-fold, generating the question about the real antioxidant role that low intracellular concentrations of vitamin C can play in the presence of a vast molar excess of glutathione. We characterized the metabolism of vitamin C and its relation...
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Published in: | The Journal of biological chemistry 2007-05, Vol.282 (21), p.15506-15515 |
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creator | Montecinos, Viviana Guzmán, Paula Barra, Valeria Villagrán, Marcelo Muñoz-Montesino, Carola Sotomayor, Kirsty Escobar, Elizabeth Godoy, Alejandro Mardones, Lorena Sotomayor, Paula Guzmán, Catherine Vásquez, Osmán Gallardo, Victoria van Zundert, Brigitte Bono, María Rosa Oñate, Sergio A. Bustamante, Marcelo Cárcamo, Juan G. Rivas, Coralia I. Vera, Juan Carlos |
description | Cellular glutathione levels may exceed vitamin C levels by 10-fold, generating the question about the real antioxidant role that low intracellular concentrations of vitamin C can play in the presence of a vast molar excess of glutathione. We characterized the metabolism of vitamin C and its relationship with glutathione in primary cultures of human endothelial cells oxidatively challenged by treatment with hydrogen peroxide or with activated cells undergoing the respiratory burst, and analyzed the manner in which vitamin C interacts with glutathione to increase the antioxidant capacity of cells. Our data indicate that: (i) endothelial cells express transporters for reduced and oxidized vitamin C and accumulate ascorbic acid with participation of glutathione-dependent dehydroascorbic acid reductases, (ii) although increased intracellular levels of vitamin C or glutathione caused augmented resistance to oxidative stress, 10-times more glutathione than vitamin C was required, (iii) full antioxidant protection required the simultaneous presence of intracellular and extracellular vitamin C at concentrations normally found in vivo, and (iv) intracellular vitamin C cooperated in enhancing glutathione recovery after oxidative challenge thus providing cells with enhanced survival potential, while extracellular vitamin C was recycled through a mechanism involving the simultaneous neutralization of oxidant species. Therefore, in endothelial cells under oxidative challenge, vitamin C functions as an essential cellular antioxidant even in the presence of a vast molar excess of glutathione. |
doi_str_mv | 10.1074/jbc.M608361200 |
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We characterized the metabolism of vitamin C and its relationship with glutathione in primary cultures of human endothelial cells oxidatively challenged by treatment with hydrogen peroxide or with activated cells undergoing the respiratory burst, and analyzed the manner in which vitamin C interacts with glutathione to increase the antioxidant capacity of cells. Our data indicate that: (i) endothelial cells express transporters for reduced and oxidized vitamin C and accumulate ascorbic acid with participation of glutathione-dependent dehydroascorbic acid reductases, (ii) although increased intracellular levels of vitamin C or glutathione caused augmented resistance to oxidative stress, 10-times more glutathione than vitamin C was required, (iii) full antioxidant protection required the simultaneous presence of intracellular and extracellular vitamin C at concentrations normally found in vivo, and (iv) intracellular vitamin C cooperated in enhancing glutathione recovery after oxidative challenge thus providing cells with enhanced survival potential, while extracellular vitamin C was recycled through a mechanism involving the simultaneous neutralization of oxidant species. Therefore, in endothelial cells under oxidative challenge, vitamin C functions as an essential cellular antioxidant even in the presence of a vast molar excess of glutathione.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M608361200</identifier><identifier>PMID: 17403685</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Antioxidants - pharmacology ; Ascorbic Acid - metabolism ; Ascorbic Acid - pharmacology ; Cell Survival - drug effects ; Dose-Response Relationship, Drug ; Endothelial Cells - metabolism ; Glutathione - pharmacology ; Humans ; Hydrogen Peroxide - pharmacology ; Oxidants - pharmacology ; Oxidation-Reduction - drug effects ; Oxidative Stress - drug effects ; Oxidoreductases - metabolism ; Respiratory Burst - drug effects</subject><ispartof>The Journal of biological chemistry, 2007-05, Vol.282 (21), p.15506-15515</ispartof><rights>2007 © 2007 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c435t-b3681f1acf24f122f3c7b26583f560c3d87a755dd0d1f7ca63f4849dddfba8d63</citedby><cites>FETCH-LOGICAL-c435t-b3681f1acf24f122f3c7b26583f560c3d87a755dd0d1f7ca63f4849dddfba8d63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0021925820874250$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3549,27924,27925,45780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17403685$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Montecinos, Viviana</creatorcontrib><creatorcontrib>Guzmán, Paula</creatorcontrib><creatorcontrib>Barra, Valeria</creatorcontrib><creatorcontrib>Villagrán, Marcelo</creatorcontrib><creatorcontrib>Muñoz-Montesino, Carola</creatorcontrib><creatorcontrib>Sotomayor, Kirsty</creatorcontrib><creatorcontrib>Escobar, Elizabeth</creatorcontrib><creatorcontrib>Godoy, Alejandro</creatorcontrib><creatorcontrib>Mardones, Lorena</creatorcontrib><creatorcontrib>Sotomayor, Paula</creatorcontrib><creatorcontrib>Guzmán, Catherine</creatorcontrib><creatorcontrib>Vásquez, Osmán</creatorcontrib><creatorcontrib>Gallardo, Victoria</creatorcontrib><creatorcontrib>van Zundert, Brigitte</creatorcontrib><creatorcontrib>Bono, María Rosa</creatorcontrib><creatorcontrib>Oñate, Sergio A.</creatorcontrib><creatorcontrib>Bustamante, Marcelo</creatorcontrib><creatorcontrib>Cárcamo, Juan G.</creatorcontrib><creatorcontrib>Rivas, Coralia I.</creatorcontrib><creatorcontrib>Vera, Juan Carlos</creatorcontrib><title>Vitamin C Is an Essential Antioxidant That Enhances Survival of Oxidatively Stressed Human Vascular Endothelial Cells in the Presence of a Vast Molar Excess of Glutathione</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Cellular glutathione levels may exceed vitamin C levels by 10-fold, generating the question about the real antioxidant role that low intracellular concentrations of vitamin C can play in the presence of a vast molar excess of glutathione. 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Our data indicate that: (i) endothelial cells express transporters for reduced and oxidized vitamin C and accumulate ascorbic acid with participation of glutathione-dependent dehydroascorbic acid reductases, (ii) although increased intracellular levels of vitamin C or glutathione caused augmented resistance to oxidative stress, 10-times more glutathione than vitamin C was required, (iii) full antioxidant protection required the simultaneous presence of intracellular and extracellular vitamin C at concentrations normally found in vivo, and (iv) intracellular vitamin C cooperated in enhancing glutathione recovery after oxidative challenge thus providing cells with enhanced survival potential, while extracellular vitamin C was recycled through a mechanism involving the simultaneous neutralization of oxidant species. 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We characterized the metabolism of vitamin C and its relationship with glutathione in primary cultures of human endothelial cells oxidatively challenged by treatment with hydrogen peroxide or with activated cells undergoing the respiratory burst, and analyzed the manner in which vitamin C interacts with glutathione to increase the antioxidant capacity of cells. Our data indicate that: (i) endothelial cells express transporters for reduced and oxidized vitamin C and accumulate ascorbic acid with participation of glutathione-dependent dehydroascorbic acid reductases, (ii) although increased intracellular levels of vitamin C or glutathione caused augmented resistance to oxidative stress, 10-times more glutathione than vitamin C was required, (iii) full antioxidant protection required the simultaneous presence of intracellular and extracellular vitamin C at concentrations normally found in vivo, and (iv) intracellular vitamin C cooperated in enhancing glutathione recovery after oxidative challenge thus providing cells with enhanced survival potential, while extracellular vitamin C was recycled through a mechanism involving the simultaneous neutralization of oxidant species. Therefore, in endothelial cells under oxidative challenge, vitamin C functions as an essential cellular antioxidant even in the presence of a vast molar excess of glutathione.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17403685</pmid><doi>10.1074/jbc.M608361200</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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source | ScienceDirect Journals; PubMed Central |
subjects | Antioxidants - pharmacology Ascorbic Acid - metabolism Ascorbic Acid - pharmacology Cell Survival - drug effects Dose-Response Relationship, Drug Endothelial Cells - metabolism Glutathione - pharmacology Humans Hydrogen Peroxide - pharmacology Oxidants - pharmacology Oxidation-Reduction - drug effects Oxidative Stress - drug effects Oxidoreductases - metabolism Respiratory Burst - drug effects |
title | Vitamin C Is an Essential Antioxidant That Enhances Survival of Oxidatively Stressed Human Vascular Endothelial Cells in the Presence of a Vast Molar Excess of Glutathione |
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