Superoxide dictates the mode of U937 cell ascorbic acid uptake and prevents the enhancing effects of the vitamin to otherwise nontoxic levels of reactive oxygen/nitrogen species. | |
MedLine Citation:
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PMID: 22633911 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Exposure of U937 cells to low micromolar levels of ascorbic acid or dehydroascorbic acid, while resulting in identical ascorbic acid accumulation, is unexpectedly associated with remarkably different responses to exogenous oxidants. We observed that otherwise nontoxic levels of hydrogen peroxide, tert-butylhydroperoxide or peroxynitrite promote toxicity in cells preloaded with ascorbic acid, whereas hardly any effect was detected in cells pretreated with dehydroascorbic acid. Further experiments performed with peroxynitrite in cells preloaded with ascorbic acid provided evidence for a very rapid nonapoptotic death, preceded by early Bax mitochondrial translocation and by mitochondrial permeability transition. The notion that conversion of extracellular ascorbic acid to dehydroascorbic acid prevents the enhancing effects on oxidant toxicity and nevertheless preserves the net amount of vitamin C accumulated was also established using ascorbate oxidase as well as various sources of superoxide, namely, xanthine/xanthine oxidase or ATP-driven NADPH oxidase activation. These findings suggest that superoxide-dependent conversion of extracellular ascorbic acid to dehydroascorbic acid represents an important component of the overall survival strategy of some cell types to reactive oxygen/nitrogen species. |
Authors:
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Mara Fiorani; Catia Azzolini; Liana Cerioni; Andrea Guidarelli; Orazio Cantoni |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-5-25 |
Journal Detail:
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Title: The Journal of nutritional biochemistry Volume: - ISSN: 1873-4847 ISO Abbreviation: - Publication Date: 2012 May |
Date Detail:
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Created Date: 2012-5-28 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9010081 Medline TA: J Nutr Biochem Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2012 Elsevier Inc. All rights reserved. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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