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• W1943404792 abstract "Clinical observations suggest that alcoholism predisposes to CCl4 hepatotoxicity. To study whether hepatic changes secondary to chronic ethanol consumption play a role, female rats were pair-fed, for 4 to 5 weeks, a nutritionally adequate liquid diet containing either ethanol (36% of total calories) or isocaloric carbohydrate (controls). CCl4 (0.5 ml per kg) was given intragastrically 15 hr after ethanol withdrawal. Within 24 hr, serum ornithine carbamyl transferase activity as well as liver lipid increased, whereas hepatic cytochrome P-450 content and the activities of hepatic aminopyrine N-demethylase and glucose-6-phosphatase decreased. All of these CCl4-induced changes were significantly greater in rats fed ethanol chronically than in their pair-fed controls. Moreover, in the ethanol-CCl4 treated animals, the activities of serum ornithine carbamyl transferase and glutamic pyruvic transaminase, and the concentration of serum bilirubin and liver lipid were significantly higher, whereas the content of hepatic cytochrome P-450, as well as the activities of hepatic aminopyrine N-demethylase and of glucose-6-phosphatase, were significantly lower than the values obtained in rats treated with CCl4 alone. These findings indicate the in vivo potentiation of CCl4 hepatotoxicity by chronic ethanol consumption, even in the absence of ethanol at the time of CCl4 administration. To study the mechanism of this ethanol-CCl4 synergism, liver microsomes were incubated with CCl4 and a reduced nicotinamide adenine dinucleotide phosphate-generating system. Destruction of cytochrome P-450 in vitro caused by CCl4 was much greater in microsomes of ethanol-treated rats than in their controls. In addition, chronic ethanol consumption increased the covalent binding of 14CCl4 metabolites to microsomal protein in vitro. Furthermore, the metabolism of 14CCl4 to 14CO2 in vitro was also found to be enhanced in the ethanol-fed rats. These results suggest that the increase of the CCl4 hepatotoxicity in chronic ethanol-fed rats is due to an enhanced microsomal activation and biotransformation of CCl4." @default.
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• W1943404792 date "1974-03-01" @default.
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• W1943404792 title "Increased Carbon Tetrachloride Hepatotoxicity, and its Mechanism, After Chronic Ethanol Consumption" @default.
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• W1943404792 doi "https://doi.org/10.1016/s0016-5085(74)80142-3" @default.
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