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.

A comparison of the effects of dietary cadmium on heart and kidney antioxidant enzymes: evidence for the greater vulnerability of the heart to cadmium toxicity.

This study demonstrates the greater susceptibility of the heart as compared to the kidney to cadmium in the presence of high dietary selenium. Male weanling rats were fed an adequate-copper low-selenium feed supplemented with 0, 10 or 50 ppm copper with or without 50 ppm dietary cadmium for 7 weeks. All rats received 0.5 ppm selenium in their drinking water. Cadmium treatment resulted in histopathological lesions in the heart, but not in the kidney. Although cadmium treatment resulted in more extensive effects on glutathione peroxidase and superoxide dismutase in the heart as compared to the kidney, no increase in peroxidation was noted in either organ, suggesting that cadmium cardiotoxicity can be dissociated from tissue peroxidation. Mean cadmium concentrations in the heart ranged from 0.55 to 1.22 micrograms cadmium g-1 tissue, wet weight, and in the kidney from 11.53 to 21.04 micrograms cadmium g-1 tissue, wet weight. In both tissues examined, cadmium levels were influenced by dietary copper and heart cadmium concentrations did not correlate with either the biochemical or histological lesions observed. Thus, tissue cadmium levels alone may not be adequate for predicting cadmium toxicity.