- Masahiko Satoh (Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University / firstname.lastname@example.org)
1) Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University , 2) Department of Environmental Health, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences , 3) Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University , 4) College of Pharmacy, Dongguk University, Korea
Cadmium (Cd) is an environmental contaminant known to exert toxic effects on various tissues. Metallothionein (MT) acts as a protective protein with high affinity for Cd. However, among the four isoforms of MT, the physiologic function of MT-III in the liver of mice exposed to Cd chronically has not been determined. In the present study, we examined the susceptibility of MT-III null mice to hepatotoxicity by exposure to Cd for 67 weeks. Cd exposure reduced the body weight of wild-type mice but not MT-III null mice. MT-I/II null mice were also exposed to Cd; as expected, they died at 18 weeks of exposure. Long-term exposure to Cd exhibited mild hepatotoxicity to wild-type mice, and the effects of MT-III on hepatotoxicity were not extensive. Long-term exposure to Cd increased mRNA levels of MT-I and MT-II in the livers of wild-type mice and MT-III null mice. These results suggest that long-term exposure to Cd may contribute similar sensitivity to the livers of MT-III null mice as that of wild-type mice because expression of MT-I and MT-II was induced in the liver of both types of mice.