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目的 探讨砷致癌的细胞分子生物学机制。方法 建立砷诱导NIH3T3细胞转化模型。测定细胞液中谷胱甘肽 (GSH)、谷胱甘肽转移酶 (GST)和谷胱甘肽还原酶 (GR)水平 ,通过NorthernBlot测定GR和谷胱甘肽过氧化物酶 (GPx)的基因表达。结果 NIH3T3细胞在 0 1 μmol/LAs(Ⅲ )诱导的 1 1 0d后发生了细胞生物学改变 ,由体外有限传代变为无限传代 ,在半固体琼脂上可以每千个细胞形成 60个集落。GR和GST活性显著增高。结论 建立了可行的砷诱导体外细胞转换的模型 ,提出了在引起细胞转化的机制中GSH的水平的下降起了重要的作用 ,而GST和GR蛋白的上升也与此机制有关。
Aim To investigate the cellular molecular biology mechanism of arsenic carcinogenesis. Methods Arsenic-induced NIH3T3 cell transformation model was established. The levels of glutathione (GSH), glutathione transferase (GST) and glutathione reductase (GR) in the cytosol were measured. The genes of GR and glutathione peroxidase (GPx) were determined by Northern blotting expression. Results NIH3T3 cells changed in cell morphology after the induction of 0 1 μmol / L As (Ⅲ) for 110 days. From limited passages to infinite passages, NIH3T3 cells could form 60 colonies per 1000 cells on semi-solid agar. GR and GST activity was significantly increased. Conclusions A viable model of arsenic-induced cell turnover in vitro was established. It is suggested that the decrease of GSH level in the mechanism of cell transformation plays an important role, and the increase of GST and GR proteins is also related to this mechanism.