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- W1936243553 abstract "Acetaminophen hepatotoxicity is believed to result from the metabolic conversion of acetaminophen to a highly reactive intermediate by cytochrome P 450. Cimetidine has been shown to be a potent inhibitor of cytochrome P 450-mediated drug metabolism in humans and in laboratory animals, -both in vivo and in vitro. Therefore, this study was undertaken to examine the possible protective effects of cimetidine administration on acetaminophen-induced hepatic necrosis in rats. We observed a striking protection against acetaminophen hepatotoxicity in cimeti dine-treated rats (120 mg/kg) up to 4 h after i.p. administration of 500 mg/kg of acetaminophen. Ci metidine-treated animals had less histologic dam age when examined by light microscopy. and they had lower serum aminotransferases than those treat ed with acetaminophen alone. Furthermore. there was less functional hepatic impairment. e.g .. im proved survival and improved ability to metabolize aminopyrine in vivo in rats receiving cimetidine compared with those receiving acetaminophen with out cimetidine. Comparison of cjmetidine treatment with N-acetylcysteine treatment of acetaminophen overdose in rats showed cimetidine as effective as N acetylcysteine, even though the dose of cimetidine given was only isth that of N-acetylcysteine on a molar basis. Cimetidine also inhibited the covalent binding of [3H]acetaminophen to hepatic micro somes in vitro, both in the presence and absence of reduced glutathione. Cimetidine did not, however," @default.
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- W1936243553 date "1981-12-01" @default.
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- W1936243553 title "Cimetidine Protects Against Acetaminophen Hepatotoxicity in Rats" @default.
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- W1936243553 doi "https://doi.org/10.1016/s0016-5085(81)80011-x" @default.
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