The Effect of Chronic Consumption of Ethanol on the Redox State of the Rat Liver

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Abstract
Isocaloric replacement of the carbohydrate content of the diet by ethanol (36% of the total caloric intake) produced fatty infiltration and a reduced redox potential of the liver. The hepatic ratio of NAD+/NADH was 1.2 in the ethanol-treated group compared to 8.6 in the pair-fed control group. This change was associated with the consumption of ethanol as, 24 h after the removal of ethanol from the liver, the ratio had returned to the level of the control group. The hepatic substrate levels of NAD+-linked lactate dehydrogenase and the NAD+-linked β-hydroxybutyrate dehydrogenase systems were measured and used to calculate the NAD+/NADH ratio of the cytoplasm and mitochondria, respectively. The chronic consumption of ethanol did not alter the ratio in the cytoplasm but did shift the ratio in the mitochondria to one-fourth that observed in the control group. Twenty-four hours after ethanol was removed from the diet, this reduced redox potential in the mitochondria shifted to a level higher than that observed in the control groups.

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