| Summary: | 碩士 === 輔仁大學 === 食品營養學系 === 94 === Excessive consumption of selenium is known to reduce the levels of reduced glutathione (GSH) and to cause damages on liver which is the most important organ for drug metabolism and detoxification for animals and humans. In this study, the HepG2 cells were selected as the model to assess the influence of Se levels on GSH levels and the related enzymes activities of drug metabolism and antioxidation. After being treated with 0, 2.5, 5, 10, 20 and 50 μM of selenium for 24, 48, or 72 hours, the viability of HepG2 cells decreased as the time and selenium concentration increased. A selenium concentration of 10 μM was needed to inhibit 50 % of cell growth. Metabolizing ≧10 μM of selenium for over 48 hours reduced the cellular levels of GSH, increased that of GSSG, thus lowered the ratio of GSH/GSSG. The results of cellular peroxide levels suggested the peroxidation with elevated medium selenium concentration. The activities of glutathione S-transferase（GST）and glutathione peroxidase（GPx）were induced with selenium concentration＜10 μM. However, the activities of glutathione reductase（GR）and superoxide dismutase（SOD）were inhibited thus altering the balance of GSH redox status. The activities of GST、QR、GPx、GR and SOD were decreased when medium selenium levels were greater than 10 μM. These observations reveal the metabolism of selenium influenced the GSH redox status and hence affecting the systems of biotransformation and antioxidation in HepG2 cells.
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