Selenium deficiency and detoxication functions in the rat: short-term effects of cadmium.

Abstract

Weanling rats were fed a Torula yeast-based selenium-deficient diet with or without supplementation of sodium selenite (0.2 ppm selenium) in the drinking water. After 5-6 weeks on the diet regimens, the liver glutathione peroxidase activity of the selenium-deficient groups had decreased to about 1% of the supplemented groups, and the rats were then used in experiments. Cadmium-induced effects on the drug-metabolizing system of the liver were measured as the microsomal capacity to perform N- and C-oxygenation of N, N-dimethylaniline. Cadmium in vitro caused a decrease of the cytochrome P-450-dependent C-oxygenation. This effect tended to be more prominent in the selenium-deficient groups. On the other hand, N-oxygenation was increased when cadmium was added in vitro, and no significant difference was found between selenium-deficient and -supplemented groups. However, as was found for the capacity to perform C-oxygenation, there was a tendency for lower N-oxygenation in the selenium-deficient rat. Lipid peroxidation, measured as thiobarbituric acid reactive substances in liver homogenates, was higher in selenium-deficient groups after in vivo treatment or in vitro addition of cadmium, and preincubation or phenobarbital induction enhanced this selenium-dependent difference. Although, the selenium-deficient rat seems more susceptible to cadmium-induced disturbances, 5-6 weeks of selenium deficiency was not enough to cause prominent impairment on the drug-metabolizing system as measured here and with the doses used in the present study.