Recurrence of Toxicity by Cadmium Released from Accumulated Cadmium-Metallothionein in Mice

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Cadmium (Cd) is a widespread toxic pollutant that enters humans and animals through the food chain. Cd usually is accumulated by binding to metallothionein (MT), which appears to be responsible for its detoxification in the cell. To investigate whether the Cd released from Cd-MT can cause toxicity to recur, we studied the effects of oxidative stress and contamination with multiple metals on the release of Cd from accumulated Cd-MT and recurrence of toxicity in vitro and in vivo. Incubation of Cd-MT with H_2O_2, ferric nitrilotriacetate (Fe-NTA) and H_2O_2, or Cu^<2+> resulted in release of Cd from its binding with MT. In vivo study, Cd was released from renal Cd-MT after mice that had accumulated Cd-MT were injected with Fe-NTA. Addition of purified Cd-MT to mouse liver cytosol did not result in inhibition of cytosolic superoxide dismutase (SOD) activity. However, treatment of Cd-MT with H_2O_2 or Cu^<2+> led to the release of Cd^<2+> from Cd-MT, which inhibited cytosolic SOD activity. Simultaneous injection with Cu^<2+> and a non-acute toxic dose of Cd significantly increased plasma aminotransferase activities, indicating hepatic injury, in mice that had accumulated Cd-MT but not in those that had accumulated Zn-MT. The hepatic concentration of Cu increased with the injected dose and the concentration of Cd in the MT fraction decreased. These results suggest that contamination with metals whose affinities for MT are higher than that of Cd may cause recurrent toxicity due to the release of Cd from accumulated Cd-MT.
公益社団法人日本薬学会の論文
2005-06-01

Recurrence of Toxicity by Cadmium Released from Accumulated Cadmium-Metallothionein in Mice

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