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Cadmium-induced alteration of drug action

Journal Article · · Fed. Proc.; (United States)
OSTI ID:5204567

Cadmium, a toxicologically important environmental contaminant, has been implicated as an etiological factor in a wide variety of pathological processes. Acute, intraperitoneal (i.p.) administration with cadmium can markedly alter the pharmacological response to a variety of drugs (hexobarbital, zoxazolamine, tremorine, and chlorpromazine) in the male rat. The threshold dose for this cadmium effect is 0.84 mg Cd/kg (i.p.) and the effect lasts at least 10 days with the peak effect occurring 2 to 5 days after cadmium. Mechanism studies reveal that the cadmium effect is the result of inhibition of hepatic drug metabolizing enzymes and not any alteration in end organ sensitivity to the drug. Treatment of male rats with cadmium prior to killing leads to a significant inhibition in the metabolism of hexobarbital, aniline, p-nitroanisole, zoxazolamine, and ethylmorphine, as well as reducing the microsomal cytochrome P-450 levels. Inhibition of the metabolism of these substrates by cadmium was also achieved when the metal was added in vitro to microsomes isolated from control rats. Pretreatment of rats with subthreshold doses of cadmium (0.21 or 0.42 mg Cd/kg, i.p.) prevented the previously observed alterations in drug action by the threshold cadmium dose. The apparent underlying basis for this protection phenomenon is the induction by cadmium of a hepatic metal-binding protein.

Research Organization:
Purdue Univ., West Lafayette, IN
OSTI ID:
5204567
Journal Information:
Fed. Proc.; (United States), Journal Name: Fed. Proc.; (United States) Vol. 37:1; ISSN FEPRA
Country of Publication:
United States
Language:
English