Effects of cadmium and dietary selenium on cytoplasmic and mitochondrial antioxidant defense systems in the heart of rats fed high dietary copper.

Rats were fed a high copper diet (50 ppm copper) supplemented with 0, 0.1 and 0.5 ppm selenium and treated with either 50 ppm cadmium admixed with their feed or given 5 mg cadmium via osmotic minipumps. Only rats fed the low-selenium basal diet and treated with cadmium via the osmotic minipumps showed a significant rise in thiobarbiturate-reactive substances. This was associated with marked reductions in the activity of the selenoenzyme, glutathione peroxidase in heart cytosol and mitochondria. Cytosolic superoxide dismutase was unaffected and catalase activity was increased as a result of cadmium treatment. Dietary cadmium also resulted in marked reductions in the activities of cytosolic glutathione peroxidase, superoxide dismutase, and catalase. These biochemical lesions were not accompanied by decreases in the corresponding mitochondrial enzymes and no increase in thiobarbiturate-reactive substances was observed. Heart metal levels indicate the formation of cadmium-selenium complexes in rats treated with cadmium via the osmotic minipumps. Dietary cadmium does not appear to interact with selenium in a similar fashion. Heart copper levels were increased by dietary cadmium treatment. Thus, heart mitochondria appear to be the site of the primary biochemical lesion for cadmium and involve increased lipid peroxidation only when mitochondrial antioxidant defense enzymes are compromised.