| Ascorbic acid improves mitochondrial function in liver of arsenic-treated rat. | |
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MedLine Citation:
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PMID: 20356860 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Arsenic is an ubiquitous and well-documented carcinogenic metalloid. The most common source of arsenic is drinking water. The mechanism of arsenic toxicity in a cell has historically been centered around its inhibitory effects on cellular respiration and mitochondrial injury. Ascorbic acid, a low molecular weight, water-soluble antioxidant, improves the reduced glutathione (GSH) status by recycling oxidized glutathione. Ascorbic acid can improve mitochondrial function by improving the thiol status; thereby preventing reactive oxygen species- mediated damage to liver as well as kidney. Ascorbic acid has been shown to protect membrane and other cellular compartments by regenerating vitamin E. Therefore, ascorbic acid seems to be a suitable protective factor against arsenic toxicity. Present reports describe the effect of ascorbic acid on oxidative phosphorylation, adenosine triphosphatase (ATPase), succinic dehydrogenase, caspase-3 and apoptosis in the liver of rats treated with arsenic trioxide (As(III)). Ultrastructural changes in the mitochondria have also been reported. We show that cotreatments with ascorbic acid and As(III) improve mitochondrial structure and function. We attribute these improvements mainly to antioxidative role of ascorbic acid. Apoptosis was restricted due to caspase-3 inhibition. Ascorbic acid could protect DNA from the attack of reactive oxygen species generated by As(III). Consequently its events led to improved ADP:O ratio, normalized ATPase activity and restored the activity of succinic dehydrogenase. Overall, results support the protective role of ascorbic acid against As( III)-induced liver injury. |
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Authors:
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Sohini Singh; Suresh Vir Singh Rana |
Publication Detail:
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Type: Journal Article Date: 2010-03-31 |
Journal Detail:
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Title: Toxicology and industrial health Volume: 26 ISSN: 1477-0393 ISO Abbreviation: Toxicol Ind Health Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-05-31 Completed Date: 2010-09-08 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8602702 Medline TA: Toxicol Ind Health Country: England |
Other Details:
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Languages: eng Pagination: 265-72 Citation Subset: IM |
Affiliation:
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Toxicology Laboratory, Department of Zoology, Ch. Charan Singh University, Meerut, India. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Diphosphate
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metabolism Adenosine Triphosphatases / metabolism Animals Arsenicals Ascorbic Acid / pharmacology* Caspase 3 / metabolism Dose-Response Relationship, Drug Histocytochemistry Liver / drug effects*, enzymology, metabolism Male Mitochondria, Liver / drug effects*, enzymology, metabolism Oxidative Phosphorylation / drug effects Oxides / toxicity* Rats Rats, Wistar Succinate Dehydrogenase / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Arsenicals; 0/Oxides; 1327-53-3/arsenic trioxide; 50-81-7/Ascorbic Acid; 58-64-0/Adenosine Diphosphate; EC 1.3.99.1/Succinate Dehydrogenase; EC 3.4.22.-/Caspase 3; EC 3.6.1.-/Adenosine Triphosphatases |
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