Effects of copper deficiency on carbon tetrachloride-induced lipid peroxidation.
To investigate the hypothesis that copper deficiency in the rat could result in increased susceptibility to CCl4-induced lipid peroxidation caused by decreased free radical defenses, we performed a series of experiments administering CCl4 to copper-deficient and control rats. Peroxidation after CCl4 administration was monitored by measuring the evolution of expired ethane in closed metabolic chambers. Rats were fed one of two copper-deficient diets based on either evaporated milk or powdered milk. Compared with control values, liver copper content, liver superoxide dismutase activity, and plasma ceruloplasmin level were significantly decreased in copper-deficient rats fed either of the diets. Liver glutathione peroxidase activity was also decreased in the copper-deficient rats fed the evaporated milk diet. Ethane evolution was markedly increased in both copper-deficient groups as compared with their controls. Copper deficiency was also found to produce increases in hepatic iron concentrations, but normal rats loaded with iron dextran to increase hepatic iron concentrations into a range similar to that found in the copper-deficient rats did not exhibit increased ethane evolution after CCl4 administration. Copper deficiency in the rat results in increased CCl4-induced lipid peroxidation.
D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000378:metabolism*; D002570:Ceruloplasmin / Q000378:metabolism; D003300:Copper / Q000172:deficiency*; D004980:Ethane / Q000378:metabolism; D005609:Free Radicals; D007501:Iron / Q000378:metabolism; D008054:Lipid Peroxides / Q000378:metabolism*; D008297:Male; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism
D005609:Free Radicals; D008054:Lipid Peroxides; D003300:Copper; D007501:Iron; D013482:Superoxide Dismutase; D002570:Ceruloplasmin; D004980:Ethane