Phenobarbital pretreatment significantly enhanced the rise in SGOT and SGPT immediately following a three-hour exposure of rats to carbon tetrachloride by inhalation. However, these parameters of hepatotoxicity were significantly lower in rats pretreated with 3-methylcholanthrene when compared to rats pretreated with vehicle and exposed to carbon tetrachloride vapor. Levels of hepatic microsomal NADPH cytochrome c reductase and CO-binding pigment were elevated by phenobarbital pretreatment, but 3-methylcholanthrene had no effect on hepatic microsomal NADPH cytochrome c reductase. Although carbon tetrachloride exposure reduced CO-binding pigment content by 61 per cent in phenobarbital pretreated and by 39 per cent in 3-methylcholanthrene pretreated rats, microsomal NADPH cytochrome c reductase was reduced by only 6 per cent and 20 per cent, respectively. In phenobarbital pretreated rats, exposure to carbon tetrachloride produced a greater decrease in aminopyrine demethylase activity than in saline treated carbon tetrachloride exposed controls. However, in 3-meteyleholanthrene pretreated rats, exposure to carbon tetrachloride produced a lesser decrease in p-nitroanisole demethylase activity than in corn oil treated controls. Twenty-one hours after exposure, the difference in SGOT and SGPT values of the phenobarbital and 3-methylcholanthrene pretreated rats was more divergent. Histological evidence at this time period revealed extensive damage in the phenobarbital pretreated. animals and a spring effect in the 3-methylcholanthrene pretreated animals.
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