Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.99.3 (diaphorase)
 5,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the presence of hepatic microsomes, styrene produced a type I difference spectrum, which demonstrates that styrene binds to the catalytic site of ferricytochrome P-450. A comparison of the binding parameters for the interaction of styrene with noninduced, phenobarbital-induced, and 3-methylcholanthrene-induced microsomes indicated that styrene is predominantly bound by cytochrome P-450 and not by cytochrome P-448. Inhalation exposure to a mixture of acetone (1,000 ppm, 6 h/d) and styrene (300 ppm, 6 h/d) for 5 d caused a distinct decrease in hepatic free nonprotein sulfhydryl groups. This decrease could be observed both with and without phenobarbital treatment. Acetone inhalation alone also enhanced ethoxycoumarin O-deethylase activity in rats without pretreatments. Acetone inhalation also increased the cytochrome P-450 content of liver microsomes, but it had no effect on NADPH cytochrome c reductase or epoxide hydratase activity. Combined exposure to styrene and acetone enhanced NADPH cytochrome c reductase activity in nonphenobarbital-treated rats, but no effect was seen in the phenobarbital-treated animals. Phenobarbital treatment of animals can greatly modify the biotransformation and toxicity of styrene, phenobarbital inducible P-450 hemoprotein playing a predominant role in its metabolism. Simultaneous inhalation exposure to acetone also interacts with the metabolism of styrene.
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PMID:Interaction of styrene and acetone with drug biotransformation enzymes in rat liver. 73 16

The purpose of this study was to determine how aging affects the induction by ethanol or acetone of the hepatic microsomal monooxygenase system of female Fischer 344 rats. Young-adult, middle-aged and old rats (4, 14 and 25 months) were fed an ethanol-containing or control liquid diet for 15 days. Cytochrome P-450, cytochrome c reductase, aniline hydroxylase, nitrophenol hydroxylase, nitroanisole O-demethylase and benzphetamine N-demethylase activities were measured in hepatic microsomes. All of the drug metabolism activities except benzphetamine N-demethylase were 20-35% lower in old than in young-adult rats fed the control diet. In addition, the increase in drug metabolism produced by feeding the regular ethanol diet (36% of calories as ethanol) was 50-60% lower in the old rats. However, there was no difference in the magnitude of ethanol induction when ethanol intakes were matched. The effects of chronic acetone consumption (1.2g/day per kg body weight for 15 days) paralleled those of ethanol consumption, except that the extent of induction was greater with acetone. Acetone-induced levels of hepatic microsomal cytochrome P-450, nitrophenol hydroxylase, nitroanisole O-demethylase and aniline hydroxylase were similar in all three age groups. The results of this study indicate that induction of hepatic microsomal drug metabolism by ethanol or acetone is unaffected by the aging process.
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PMID:Effects of ethanol on microsomal drug metabolism in aging female rats. I. Induction. 273 65