Abstract
There is evidence to suggest that the mechanism of antioxidant effect of prostaglandin E1 (PGE1) is due to decrease of radical species generation by cytochrome P-450 in rat liver microsomes. Chronic alcohol intoxication increased NADPH oxidation, cytochrome P-450 content and NADPH-stimulated chemoluminiscence of microsomes. Ethanol also raised superoxide dismutase (SOD) activity in microsomes. PGE1 decreased cytochrome P-450 content, normalized NADPH oxidation, NADPH-induced chemoluminiscence and SOD activity in the liver of alcohol-treated rats. PGE developed the similar effect after microsomal induction by both acetone combined with starvation and phenobarbital normalizing all the above parameters. Therefore, PGE1 affects on both, ethanol-inducible IIE1 and phenobarbital-inducible IIB1 isoforms.
MeSH terms
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Acetone / administration & dosage
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Alprostadil / administration & dosage
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Alprostadil / pharmacology*
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Animals
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Cytochrome P-450 CYP2B1 / metabolism*
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Cytochrome P-450 CYP2E1 / metabolism*
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Down-Regulation
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Ethanol / administration & dosage
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Free Radicals / metabolism*
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Hydrogen Peroxide / metabolism
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Luminescent Measurements
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Male
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Microsomes, Liver / drug effects
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Microsomes, Liver / enzymology*
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NADH, NADPH Oxidoreductases / metabolism
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NADP / metabolism
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NADPH Oxidases / metabolism
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Phenobarbital / administration & dosage
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Rats
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Rats, Inbred Strains
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Starvation / enzymology
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Superoxide Dismutase / metabolism
Substances
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Free Radicals
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Acetone
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Ethanol
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NADP
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Hydrogen Peroxide
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Cytochrome P-450 CYP2E1
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Cytochrome P-450 CYP2B1
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Superoxide Dismutase
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NADH, NADPH Oxidoreductases
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NADH-cytochrome P-450 reductase
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NADPH Oxidases
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Alprostadil
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Phenobarbital