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175. CYP2C11 and CYP2B1 are major cytochrome P450 forms involved in styrene oxidation in liver and lung microsomes from untreated rats, respectively

Author

Wang Rui-Sheng, Harry V. Gelboin, Frank J. Gonzalez, Harri Vainio, E. Elovaara, Nakajima Tamie, and Aoyama Toshifumi

Subjects
Male, Cytochrome, Biochemistry, Styrene, Styrenes, chemistry.chemical_compound, Cytochrome P-450 Enzyme System, Microsomes, Animals, Cytochrome P-450 Enzyme Inhibitors, Enzyme inducer, Rats, Wistar, Lung, Pharmacology, Ethanol, biology, Cytochrome P450, Antibodies, Monoclonal, Metabolism, CYP2E1, Molecular biology, Rats, Isoenzymes, chemistry, Enzyme Induction, Steroid Hydroxylases, biology.protein, Microsome, Microsomes, Liver, Ethylene Glycols, Aryl Hydrocarbon Hydroxylases, Oxidation-Reduction
Abstract

The contribution of cytochrome P450s (P450s) to the formation of styrene glycol from styrene in rat liver microsomes was investigated using monoclonal antibodies to P450s. Anti-CYP2E1 inhibited the formation to a similar extent in ethanol-treated microsomes and in control microsomes in terms of percentage inhibition, whereas to a greater extent in the former than the latter in terms of net inhibition, and only at low substrate concentration. Anti-CYP2C11/6 also inhibited the formation in control and in ethanol-treated microsomes at both low and high concentrations of styrene, and the net degree of inhibition was greater than that obtained with anti-CYP2E1, even in ethanol-treated microsomes where CYP2E1 was induced. Anti-CYP2B1/2 and anti-CYP1A1/2 inhibited the formation only in phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced microsomes, respectively. These results suggest that (1) at least four P450s, CYP2C11/6, CYP2E1, CYP2B1/2 and CYP1A1/2, contribute to the metabolism of styrene, (2) CYP2C11/6, which probably corresponds to CYP2C11, is the major form of P450 responsible for the metabolism in untreated rat liver microsomes, and also in those treated with ethanol. Anti-CYP2E1 inhibited styrene oxidation more prominently in microsomes from styrene-treated rats than in those from control rats at a low substrate concentration. Although styrene treatment did not influence the total metabolism of styrene in liver microsomes at a high substrate concentration, inhibition of the metabolism by anti-CYP2C11/6 decreased with increasing styrene dose, whereas that by anti-CYP2B1/2 increased, suggesting that styrene treatment increases CYP2B1/2 but decreases CYP2C11/6 in rat liver, and the major form of P450 which mediates styrene oxidation is CYP2B1/2 after the treatment. Only anti-CYP2B1/2, which probably corresponds to CYP2B1, inhibited styrene oxidation in lung microsomes from untreated and even styrene-treated rats. Thus, the major form of P450 responsible for the metabolism of styrene is different in each tissue.

Published
1994

191. Enhancement of ethanol-induced lipid peroxidation in rat liver by lowered carbohydrate intake

Author

Nakajima Tamie, Ikatsu Hisayoshi, Murayama Ninzo, Okino Tomonori, Wang Rui-Sheng, Yonekura Ikumi, and Sato Akio

Subjects
Male, medicine.medical_specialty, Biochemistry, Hemolysis, Lipid peroxidation, Microsomal ethanol oxidizing system, chemistry.chemical_compound, Cytochrome P-450 Enzyme System, Internal medicine, Malondialdehyde, medicine, Dietary Carbohydrates, Animals, Triglycerides, Pharmacology, Ethanol, Chemistry, Body Weight, Proteins, Rats, Inbred Strains, Glutathione, Organ Size, Carbohydrate, Rats, Endocrinology, Liver, Toxicity, Microsome, Microsomes, Liver, Lipid Peroxidation, Energy Intake
Abstract

In order to investigate the effect of carbohydrate intake on ethanol-induced lipid peroxidation and cytotoxicity, rats were maintained on four different test diets, a medium-carbohydrate (carbohydrate intake, 8.4 g/day/rat on average), a low-carbohydrate (carbohydrate intake, 2.8 g/day/rat on average), an ethanol-containing medium-carbohydrate (carbohydrate and an ethanol intake, 8.4 and 2.9 g/day/ rat on average, respectively), and an ethanol-containing low-carbohydrate diet (2.8 and 2.9 g/day/rat on average, respectively). Ethanol and the low-carbohydrate diet each increased the liver malondialdehyde content, but the combined effect of both (ethanol-containing low-carbohydrate diet) was much more prominent than either alone. The degree of increase in malondialdehyde content almost paralleled the activity of the microsomal ethanol oxidizing system. Both the low-carbohydrate and the ethanol-containing low-carbohydrate diets decreased the liver glutathione content, but ethanol combined with the medium-carbohydrate diet had no effect on the content. Ethanol treatment increased the liver triglyceride content only when combined with the low-carbohydrate diet. The rate of NADPH-dependent microsomal malondialdehyde formation was much higher in microsomes from rats maintained on the ethanol-containing low-carbohydrate diet than in those from rats on the ethanol-containing medium-carbohydrate diet, indicating that lowered carbohydrate intake augments ethanol-induced malon-dialdehyde accumulation in the liver by enhancing the rate of lipid peroxidation. In addition, when incubated with red blood cells in the presence of NADPH, microsomes from rats fed the ethanol-containing low-carbohydrate diet caused marked hemolysis, which was prevented by the addition of 5mM glutathione to the incubation system. Furthermore, addition of 50 mM ethanol to the reaction system greatly accentuated the hemolysis. These results suggest that lowered carbohydrate intake at the time of ethanol consumption potentiates ethanol cytotoxicity by enhancing ethanol-induced lipid peroxidation.

Published
1992

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