2005 Volume 16 Issue 4 Pages 336-340
Cadmium nitrate (CN) is generally used for Ni-Cd batteries in industrial fields. However, there are no reports on the acute lethal toxicity of CN. LD50 and LD90 were 7.2 mg/kg and 8.1 mg/kg, respectively, after a single intravenous injection of CN in rats. A dose of CN (2.7, 5.4, 8.1 (mg/kg)) or saline (control) was intravenously administered to investigate the kinetics of cadmium (Cd) in blood and bile and dose-dependent hepatic damage after 5 hours. Liver dysfunction was caused in a dose-dependent manner and hepatic injury was severe in the 8.1 mg/kg group. The changes in serum Cd concentrations and kinetic parameters indicated that the clearance of Cd was significantly altered in the 8.1 mg/kg group. The excretion of Cd in the bile increased in the 8.1 mg/kg group. It indicated that Cd was transported in blood and Cd induces the synthesis of metallothionein and would be stored in the liver as a Cd-MT complex; however, when the Cd dose greatly exceeds the its ability to accumulate in the liver, bile excretion of cadmium increases. We suggest that the Cd binding sites in the liver were saturated and that more Cd was available for biliary excretion in the 8.1 mg/kg group. Detoxication after acute CN exposure would be dependent upon accumulation of Cd in the liver. Severe liver dysfunction was caused by acute exposure to high concentration of CN that exceed the accumulation of the liver and it caused reduction of clearance of Cd.
