M. Fields et al., ANTIOXIDANT DEFENSE-MECHANISMS IN THE MALE-RAT - INTERACTION WITH ALCOHOL, COPPER, AND TYPE OF DIETARY CARBOHYDRATE, Alcohol, 12(1), 1995, pp. 65-70
The activities of enzymes participating in cellular protection against
free radical reactions were measured in hepatic tissues from copper-a
dequate and copper-deficient rats fed fructose or starch-based diets.
Half of the rats consumed 20% ethanol in their drinking water. The con
sumption of ethanol depressed growth rate, reduced hematocrit, and hep
atic copper concentration. Feed efficiency was greatly depressed by et
hanol. Mortality due to copper deficiency occurred in fructose-fed rat
s and in starch-fed rats that drank ethanol. Ethanol had no effect on
superoxide dismutase (SOD), glutathione peroxidsase (GSH-Px), or catal
ase. In contrast, copper deficiency reduced SOD and fructose feeding d
epressed catalase activity. GSH-Px was not affected by either the type
of dietary carbohydrate, copper, or ethanol. Taken together, these da
ta suggest that additional mechanisms to antioxidant defense systems a
re responsible for the metabolic changes that occur during the interac
tions between ethanol low copper and dietary carbohydrates.