• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.6
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• pp.894-898
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• 1994

To evaluate an effect of dietary protein on the liver damage, the bromobenzene was intraperitoneally injected to the rats fed a low or high protein diet and then the liver weight per body weight and serum levels of alanine aminotransferase (ALT) activities were determined to demonstrate the differences in liver damage between the groups fed low or high protein diet. Hepatic aniline hydroxylase (AH), glutthione (GSH) content and glutathione s-transferase(GST) activity were also determined to clarify causes of liver damage between the two groups. Increases of liver weight per body weight and serum ALT activities were higher in brombenzene treated rats fed low protein diet than those fed high protein diet. The increasing rate of hepatic AH activity was higher in bromobenzne-treated rats fed low protein diet than that in those fed high protein diet. Furthermore , hepatic glutathione contents and GST activities in bromobenzene-treated rats were higher in rats fed high protein diet than those fed low protein diet. In case of control group, the heaptic glutathione content and GST activity were also higher in rats fed high protein diet than those fed low protein diet.

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.6
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• pp.702-708
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• 1993

The study was attempted to elucidate the mechanism of GE-132(100mg/kg, p.o. for 6 weeks) on the metabolism of bromobenzene (460mg/kg, i.p. bid, for 2 days), which has potent carcinogenicity, mutagenicity and hepatotoxicity. It showed that activities of cytochrome p-450, aminopyrine demethylase and aniline hydroxylase, which have epoxide generating property, were not changed by GE-132 treatment. On the other hand, epoxide hydrolase was not changed but that glutathione S-transferase was significantly increased by GE-132 treatment. And also ${\gamma}-glutamylcysteine$ synthetase was not changed following the GE-132 treatment, but the activity of glutathione reductase was significantly increased. The level of hepatic glutathione which was decreased by bromobenzene recovered markedly by GE-132 pretreatment. It is concluded that the mechanism for the observed effect of GE-132 on bromobenzene metabolism is due to the induction of glutathione S-transferase.