Objective To study the effects of selenium on DNA damage, apoptosis and c-myc, c-fos, and c-jun expression in rat hepatocytes. Methods Sodium selenite at the doses of 5, 10, and 20 μmol/kg was given to rats by i.p. a...Objective To study the effects of selenium on DNA damage, apoptosis and c-myc, c-fos, and c-jun expression in rat hepatocytes. Methods Sodium selenite at the doses of 5, 10, and 20 μmol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was detected by single cell gel electrophoresis （or comet assay）. Hepatocellular apoptosis was determined by TUNEL （TdT-mediated dUTP nick end labelling） and flow cytometry. C-myc, c-fos, and c-jun expression in rat bepatocytes were assayed by Northern dot hybridization. C-myc, c-fos, and c-jun protein were detected by immunohistochemical method. Results At the doses of 5, 10, and 20μmol/kg, DNA damage was induced by sodium selenite in rat hepatocytes and the rates of comet cells were 34.40%, 74.80%, and 91.40% respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the doses of sodium selenite （r=0.9501, P〈0.01）. Sodium selenite at the doses of 5, 10, and 20μmol/kg caused c-myc, c-fos, and c-jun overexpression obviously. The positive brown-yellow signal for proteins of c-myc, c-fos, and c-jun was mainly located in the cytoplasm of bepatocytes with immunohistocbemical method. TUNEL-positive cells were detected in selenium-treated rat livers. Apoptotic rates （%） of selenium-treated liver cells at the doses of 5, 10, and 20 μmol/kg were （3.72±1.76）, （5.82±1.42）, and （11.76±1.87） respectively, being much higher than those in the control. Besides an obvious dose-response relationship between apoptotic rates and the doses of sodium selenite （r=0.9897, P〈0.01）, these results displayed a close relationship between DNA damage rates and apoptotic rates, and the relative coefficient was 0.9021, P〈0.01. Conclusion Selenium at 5-20μmol/kg can induce DNA damage, apoptosis, and overexpression of c-myc, c-fos, and c-jun in rat hepatocytes.展开更多
基金This work was supported by National Natural Science Foundation of China (No. 30271110, 30471500).
文摘Objective To study the effects of selenium on DNA damage, apoptosis and c-myc, c-fos, and c-jun expression in rat hepatocytes. Methods Sodium selenite at the doses of 5, 10, and 20 μmol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was detected by single cell gel electrophoresis （or comet assay）. Hepatocellular apoptosis was determined by TUNEL （TdT-mediated dUTP nick end labelling） and flow cytometry. C-myc, c-fos, and c-jun expression in rat bepatocytes were assayed by Northern dot hybridization. C-myc, c-fos, and c-jun protein were detected by immunohistochemical method. Results At the doses of 5, 10, and 20μmol/kg, DNA damage was induced by sodium selenite in rat hepatocytes and the rates of comet cells were 34.40%, 74.80%, and 91.40% respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the doses of sodium selenite （r=0.9501, P〈0.01）. Sodium selenite at the doses of 5, 10, and 20μmol/kg caused c-myc, c-fos, and c-jun overexpression obviously. The positive brown-yellow signal for proteins of c-myc, c-fos, and c-jun was mainly located in the cytoplasm of bepatocytes with immunohistocbemical method. TUNEL-positive cells were detected in selenium-treated rat livers. Apoptotic rates （%） of selenium-treated liver cells at the doses of 5, 10, and 20 μmol/kg were （3.72±1.76）, （5.82±1.42）, and （11.76±1.87） respectively, being much higher than those in the control. Besides an obvious dose-response relationship between apoptotic rates and the doses of sodium selenite （r=0.9897, P〈0.01）, these results displayed a close relationship between DNA damage rates and apoptotic rates, and the relative coefficient was 0.9021, P〈0.01. Conclusion Selenium at 5-20μmol/kg can induce DNA damage, apoptosis, and overexpression of c-myc, c-fos, and c-jun in rat hepatocytes.
