Sodium selenite-induced oxidative stress and apoptosis in human hepatoma HepG2 cells

✍ Scribed by Han-Ming Shen; Cheng-Feng Yang; Choon-Nam Ong

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: French
• Weight: 385 KB
• Volume: 81
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/(sici)1097-0215(19990531)81:5<820::aid-ijc25>3.0.co;2-f

✦ Synopsis

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 (HepG 2 ). Sodium selenite (10 M) exerted clear cytotoxic effect, as shown by the significant increase of lactate dehydrogenase leakage. Seleniteinduced 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 seleniteinduced 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.