| Sodium selenite-induced oxidative stress and apoptosis in human hepatoma HepG2 cells. | |
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MedLine Citation:
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PMID: 10328239 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The mechanisms involved in the anti-carcinogenic activity of selenium remain to be elucidated. In the present study, we examined sodium selenite-induced oxidative stress and apoptosis in a human hepatoma cell line (HepG2). Sodium selenite (10 microM) exerted clear cytotoxic effect, as shown by the significant increase of lactate dehydrogenase leakage. Selenite-induced DNA alterations in apoptosis were studied by: 1. comet assay; 2. TdT-mediated dUTP nick end-labeling assay. In addition, characteristic apoptotic morphological alterations were also observed in selenite-treated cells. Our results clearly show that Se-induced cell death occurs predominantly in the form of apoptosis. Selenite-induced oxidative stress was evaluated by the measurement of reactive oxygen species production using lucigenin-dependent chemiluminescence. The involvement of glutathione in selenite-induced oxidative stress was further demonstrated by the concurrent decline of intracellular reduced glutathione and increase of oxidized glutathione contents in Se-treated cells. Moreover, the finding that selenite-induced oxidative stress and apoptosis was significantly attenuated by superoxide dismutase, catalase and deferoxamine provides additional evidence to suggest that Se-induced oxidative stress mediates the induction of apoptosis, a mechanism related to the anti-carcinogenic and chemopreventive effect of Se. |
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Authors:
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H M Shen; C F Yang; C N Ong |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: International journal of cancer. Journal international du cancer Volume: 81 ISSN: 0020-7136 ISO Abbreviation: Int. J. Cancer Publication Date: 1999 May |
Date Detail:
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Created Date: 1999-06-25 Completed Date: 1999-06-25 Revised Date: 2007-07-24 |
Medline Journal Info:
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Nlm Unique ID: 0042124 Medline TA: Int J Cancer Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 820-8 Citation Subset: IM |
Affiliation:
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Department of Community, Occupational and Family Medicine, Faculty of Medicine, National University of Singapore, Republic of Singapore. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis* Carcinoma, Hepatocellular / metabolism*, pathology Catalase / pharmacology Deferoxamine / pharmacology Dose-Response Relationship, Drug Glutathione / metabolism Glutathione Disulfide / metabolism Humans In Situ Nick-End Labeling Intracellular Fluid / drug effects, metabolism L-Lactate Dehydrogenase / metabolism Oxidative Stress / drug effects* Reactive Oxygen Species / metabolism Sodium Selenite / pharmacology* Superoxide Dismutase / pharmacology Time Factors Tumor Cells, Cultured |
| Chemical | |
Reg. No./Substance:
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0/Reactive Oxygen Species; 10102-18-8/Sodium Selenite; 27025-41-8/Glutathione Disulfide; 70-18-8/Glutathione; 70-51-9/Deferoxamine; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 1.11.1.6/Catalase; EC 1.15.1.1/Superoxide Dismutase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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