Alcohol consumption aggravates copper deficiency.

Male weanling Sprague-Dawley rats were fed a copper-deficient (0.6 microgram Cu/g) diet containing either fructose or starch. Half of the animals fed the starch diet drank a 20% solution of ethanol in water. Ethanol was chosen as an agent to mimic fructose metabolism with the intention that ethanol will exacerbate the signs of copper deficiency and will negate the protective effect of dietary starch. The consumption of a 20% ethanol drink for 6 weeks by copper-deficient rats fed starch resulted in the exacerbation of the deficiency similar to that exerted by fructose. The signs associated with the deficiency in both alcohol and fructose consumption included anemia, heart hypertrophy with gross abnormalities, and mortality. In contrast, none of the copper-deficient control rats that drank water exhibited anemia or heart abnormalities, and none died of the deficiency. In addition, sorbitol pathway in the kidney and liver was stimulated by the consumption of alcohol and fructose. The data support the contention that the combination of certain metabolic pathways of carbohydrate metabolism with copper deficiency are responsible for the exacerbation of the deficiency.