Depressed hepatic glutathione and increased diene conjugates in alcoholic liver disease : Evidence of lipid peroxidation

Prolonged consumption of ethanol enhances the activities of the hepatic microsomal ethanol oxidizing system and of reduced nicotinamide-adenine dinucleotide phosphate oxidase, but not of catalase. The oxidase-catalase system is not part of the microsomal ethanol oxidizing system since catalase inhibitors dissociate ethanol oxidation by the two pathways. Enhanced reduced nicotinamide-adenine dinucleotide phosphate oxidase activity may contribute to liver injury, possibly by favoring lipoperoxidation.