Alteration of chemically induced hepatotoxicity by copper (II) (3,5-diisopropylsalicylate)2.
The effects of copper (II) (3,5-diisopropylsalicylate)2 (CuDIPS), which is a synthetic superoxide dismutase, on the hepatotoxicity of carbon tetrachloride and acetaminophen in fed and fasted animals were investigated. CuDIPS did not alter the covalent binding of metabolites of either of these chemicals to the hepatic endoplasmic reticulum. However, CuDIPS did inhibit the hepatotoxicity of carbon tetrachloride by inhibiting the induction of lipid peroxidation by carbon tetrachloride. CuDIPS had only a slight, and histologically insignificant, ability to decrease acetaminophen hepatotoxicity which is related to the inability of CuDIPS to prevent depletion of reduced glutathione by acetaminophen. The observation that fasting potentiates the hepatotoxicity of acetaminophen is emphasized, and the mechanism of this potentiation is suggested to be related to the depletion of reduced glutathione.
D000082:Acetaminophen / Q000633:toxicity; D000818:Animals; D000970:Antineoplastic Agents / Q000633:toxicity*; D002251:Carbon Tetrachloride / Q000633:toxicity; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000187:drug effects*; D008297:Male; D051379:Mice; D051381:Rats; D011919:Rats, Inbred Strains; D012459:Salicylates / Q000633:toxicity*; D013481:Superoxides / Q000378:metabolism
D000970:Antineoplastic Agents; D008054:Lipid Peroxides; D012459:Salicylates; D013481:Superoxides; C030865:copper bis(3,5-diisopropylsalicylate); D000082:Acetaminophen; D002251:Carbon Tetrachloride