Abstract
Chloroform (CHCl 3) administered to phenobarbital-pretreated rats decreased liver glutathione (GSH) and caused massive liver necrosis. Only those doses of CHCl 3 that decreased GSH in the liver caused centrilobular liver necrosis. Other halogenated alkanes studied, including CCl 4 and CCl 3Br, did not deplete liver GSH in phenobarbital-pretreated rats. In rats pretreated with 3-methylcholanthrene, isopropyl alcohol, or acetone, which also increase drug metabolism, CHCl 3 did not markedly decrease GSH in the liver. The GSH depletion was not due to oxidation of GSH or to inhibition of GSH reductase because CHCl 3 administration did not increase the amount of oxidized GSH in liver, whole blood, or kidney. Since only liver GSH was depleted in these experiments, it appeared that depletion was related to CHCl 3 metabolism. Since CCl 4 and CCl 3Br are postulated to form the trichloromethyl-free radical (CCl 3·), and since these compounds do not deplete liver GSH in phenobarbital-pretreated rats, the GSH depletion by CHCl 3 may be due to formation of chemically reactive metabolites other than the trichloromethyl free radical.
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