Antioxidant defense mechanisms in the male rat: interaction with alcohol, copper, and type of dietary carbohydrate.

The activities of enzymes participating in cellular protection against free radical reactions were measured in hepatic tissues from copper-adequate and copper-deficient rats fed fructose or starch-based diets. Half of the rats consumed 20% ethanol in their drinking water. The consumption of ethanol depressed growth rate, reduced hematocrit, and hepatic copper concentration. Feed efficiency was greatly depressed by ethanol. Mortality due to copper deficiency occurred in fructose-fed rats and in starch-fed rats that drank ethanol. Ethanol had no effect on superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), or catalase. In contrast, copper deficiency reduced SOD and fructose feeding depressed catalase activity. GSH-Px was not affected by either the type of dietary carbohydrate, copper, or ethanol. Taken together, these data suggest that additional mechanisms to antioxidant defense systems are responsible for the metabolic changes that occur during the interactions between ethanol low copper and dietary carbohydrates.