Abstract
Abstract
Copper sulfate injected intraperitoneally at a dose of 2 mg Cu/kg into vitamin E-and selenium-deficient rats caused a sixfold increase in the formation in vivo of the lipid peroxidation product ethane, and caused acute mortality in 4/5 rats. Selenium supplementation of the diet at 0.5 ppm Se largely prevented the increase in ethane production caused by copper injection and reduced mortality to 1/5 rats. Vitamin E supplementation of the diet at 200 IU/kg fully eliminated the increase in ethane production caused by copper injection, and completely prevented mortality. Vitamin E-deficient rats injected with copper sulfate at 5 mg Cu/kg produced over 10 times the ethane produced by rats injected with sodium sulfate or left uninjected. The ethylene produced by the rats injected with copper sulfate was 5% of the ethane produced, and did not differ significantly from the ethylene produced by the controls. Adding copper sulfate at 5 ppm Cu to a liver homogenate stimulated the production of ethane but not of ethylene. The correlation of increased ethane production with increased mortality suggests that lipid peroxidation may be important in the increased toxicity of copper in vitamin E- and selenium-deficient rats.
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