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|dc.title||Sodium selenite-induced oxidative stress and apoptosis in human hepatoma HepG2 cells|
|dc.identifier.citation||Shen, H.-M.,Yang, C.-F.,Ong, C.-N. (1999). Sodium selenite-induced oxidative stress and apoptosis in human hepatoma HepG2 cells. International Journal of Cancer 81 (5) : 820-828. ScholarBank@NUS Repository. <a href="https://doi.org/10.1002/(SICI)1097-0215(19990531)81:53.0.CO;2-F" target="_blank">https://doi.org/10.1002/(SICI)1097-0215(19990531)81:53.0.CO;2-F</a>|
|dc.description.abstract||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.|
|dc.contributor.department||COMMUNITY,OCCUPATIONAL & FAMILY MEDICINE|
|dc.description.sourcetitle||International Journal of Cancer|
|Appears in Collections:||Staff Publications|
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