Effect of Dietary Ethanol and Cholesterol on Metabolic Functions of Hepatic Mitochondria and Microsomes from the Monkey, Macaca nemestrina

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Abstract
Monkeys (M. nemestrina) were divided into 4 groups, and each group was fed a particular diet. The variables in the diets were as follows: diet A, 0.3 mg cholesterol/kcal nutrient; diet B, 1.0 mg cholesterol/kcal nutrient; diet C 0,3 mg cholesterol/kcal nutrient, ethanol (36% of calories); diet D, 10 mg cholesterol/kcal nutrient, ethanol (36% of calories). Monkeys on the diets containing ethanol developed fatty liver. Mitochondria from ethanol-fed animals demonstrated significant decreases in uncoupler-stimulated state 3 and state 4 succinate oxidation activity, respiratory control ratio and ATP content. Liver microsomes isolated from the ethanol-fed groups demonstrated increased ethanol oxidizing activity with NADPH or H2O2 as cosubstrate. Aniline hydroxylase and aminopyrine-N-demethylase activities were also elevated in ethanol-fed animals. The alterations in these functional properties were related primarily to ethanol in the diets. Cholesterol, while being less of a perturbant than ethanol, did elicit a significant decrease in cytochrome oxidase activity of mitochondria and a small but statistically significant increase in microsomal-associated ethanol oxidation activity. It potentiated the effect of ethanol in lowering mitochondrial respiratory control and ATP concentrations.