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

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 μM) 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. Int. J. Cancer 81:820–828, 1999. © 1999 Wiley‐Liss, Inc.