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Cadmium is one of the well-known environmental toxicants and induces cancer in rodents and human, but its carcinogenic mechanism has not been well demonstrated until now. Genotoxic effects of cadmium in Salmonella typhimurium TA98, TA100 and TA1535/pSK1002 or in WB-F344 rat liver epithelial cells were investigated to elucidate the tumor initiating effects of cadmium. TA98, TA100 and TA1535/pSK1002 tester strains were used to detect frameshift mutation, base-pair mutation and SOS repair response, respectively, in Salmonella mutation test. Reverse mutations from histidine to histidine^+ of Salmonella typhimurium TA98 and TA100 by CdCl₂ were not significantly different from control up to the maximum doses (100μM and 200μM in TA98 and TA100, respectively) at which non-cytotoxicity was observed. DNA SOS repair responses(β-galactosidase activity) generally did not show significant increases compared to control in both of the conditions with or without metabolic activation in Salmonella typhimurium TA1535/pSK1002 by CdCl₂. But the activities of β-galactosidase by 400μM of CdCl₂ in metabolic activation condition and by 130 and 400μM of CdCl₂ in non-metabolic activation condition were more decreased than those of control. DNA single strand breaks for 4hrs were observed only in WB-F344 rat liver epithelial cells treated with 200μM of CdCl₂. As a conclusion, CdCl₂ did not induce gene mutation in microbials but induce DNA single strand breaks in rat liver epithelial cells.
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