Document Detail

Sodium selenite-induced oxidative stress and apoptosis in human hepatoma HepG2 cells.
MedLine Citation:
PMID:  10328239     Owner:  NLM     Status:  MEDLINE    
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.
H M Shen; C F Yang; C N Ong
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
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:
Created Date:  1999-06-25     Completed Date:  1999-06-25     Revised Date:  2007-07-24    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  820-8     Citation Subset:  IM    
Department of Community, Occupational and Family Medicine, Faculty of Medicine, National University of Singapore, Republic of Singapore.
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MeSH Terms
Carcinoma, Hepatocellular / metabolism*,  pathology
Catalase / pharmacology
Deferoxamine / pharmacology
Dose-Response Relationship, Drug
Glutathione / metabolism
Glutathione Disulfide / metabolism
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
Reg. No./Substance:
0/Reactive Oxygen Species; 10102-18-8/Sodium Selenite; 27025-41-8/Glutathione Disulfide; 70-18-8/Glutathione; 70-51-9/Deferoxamine; EC Dehydrogenase; EC; EC Dismutase

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