Objective To study the effects of cadmium on hepatocellular DNA damage,expression of proto-oncogenes c-myc,c-fos,and c-jun as well as apoptosis in rats. Methods Cadmium chloride 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 measured by single cell gel electrophoresis(or comet assay),while expression of proto-oncogenes c-myc,c-fos,and c-jun in rat hepatocytes were measured by Northern dot hybridization. C-Myc,c-Fos,and c-Jun were detected with immuno-histochemical method. Hepatocellular apoptosis was determined by TUNEL(TdT-mediated dUTP Nick End Labelling) and flow cytometry. Results At the doses of 5,10,and 20 μmol/kg,cadmium chloride induced DNA damage in rat hepatocytes and the rates of comet cells were 50.20%,88.40%,and 93.80%,respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the dose of cadmium chloride(r =0.9172,P<0.01). Cadmium chloride at the doses of 5,10,and 20 μmol/kg induced expression of proto-oncogenes c-myc,c-fos,and c-jun. The positive brown-yellow signal for c-myc,c-fos,and c-jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in cadmium-treated rat livers. Apoptotic rates(%) of cadmium-treated liver cells at the doses of 5,10,and 20 μmol/kg were(17.24 ±2.98),(20.58±1.35),and(24.06±1.77) respectively,being significantly higher than those in the control. The results also displayed an obvious dose-response relationship between apoptotic rates and the dose of cadmium chloride(r=0.8619,P<0.05). Conclusion Cadmium at 5-20 μmol/kg can induce hepatocellular DNA damage,expression of proto-oncogenes c-myc,c-fos,and c-jun as well as apoptosis in rats. Objective To study the effects of cadmium on hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats. Methods Cadmium chloride at the doses of 5, 10, and 20 μmol / kg was given to rats by ip and there were 5 male SD rats in each group. Hepatocellular DNA damage was measured by single cell gel electrophoresis (or comet assay), while expression of proto-oncogenes c-myc, c-fos, and c-Jun in rat hepatocytes were measured by Northern dot hybridization. C-Myc, c-Fos, and c-Jun were detected with immuno-histochemical method. Hepatocellular apoptosis was determined by TUN-TdT- mediated dUTP Nick End Labeling and flow Results At the doses of 5, 10, and 20 μmol / kg, cadmium chloride induced DNA damage in rat hepatocytes and the rates of comet cells were 50.20%, 88.40%, and 93.80% respectively. -response relationship between the rates of comet cells and the dose of cadmium chloride (r = 0.9172, P <0.01). Cadmium c hloride at the doses of 5, 10, and 20 μmol / kg induced expression of proto-oncogenes c-myc, c-fos, and c-jun. The positive brown-yellow signal for c-myc, c-fos, and c -jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in cadmium-treated rats livers. Apoptotic rates (%) of cadmium-treated liver cells at doses of 5, 10, and 20 μmol / kg were (17.24 ± 2.98), (20.58 ± 1.35), and (24.06 ± 1.77) respectively, were significantly higher than those in the control. The results also displayed an obvious dose-response relationship between apoptotic rates and the dose of cadmium chloride (r = 0.8619, P <0.05). Conclusion Cadmium at 5-20 μmol / kg can induce hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.