Selenium deficiency and detoxication functions in the rat: effect of chronic dietary cadmium

Male rats from moderately selenium-deficient dams were fed a Torula yeast-based, selenium-deficient diet for 7 weeks, with or without added supplements of sodium selenite (0.2 ppm selenium) and cadmium chloride (50 ppm cadmium) in the drinking water. Cadmium caused about 10% body-weight loss in selenium-deficient, as well as in supplemented rats. Glutathione peroxidase activity in liver 105,000 g supernatant and in erythrocyte hemolysate from selenium-deficient rats was about 1% and 3%, respectively, of that in supplemented rats. A cadmium-induced decrease of glutathione peroxidase activity was found in erythrocyte and liver preparations from selenium-supplemented rats, while cadmium caused an increase of the liver activity in selenium deficiency. Selenium deficiency per se caused a significant decrease of cytochrome P-450 content, while cadmium treatment did not modify further the content of this enzyme. NADPH-cytochrome c reductase was not changed by selenium regimen or cadmium treatment, while cytochrome b5 was increased on cadmium treatment of the supplemented rat. The microsomal metabolism of N,N-dimethylaniline showed a decrease of the cytochrome P-450-dependent C-oxygenation in selenium-deficient groups. Cadmium treatment had no further significant effect. The flavin-containing monooxygenase, which performs N-oxygenation of N,N-dimethylaniline, was decreased significantly by cadmium treatment in selenium deficiency. Selenium deficiency seems thus to be connected with higher susceptibility to cadmium-induced impairments of liver detoxication functions, although progressive accumulation of cadmium in the liver appears to produce only modest effects.