Effect of chronic ethanol ingestion on the metabolism of copper, iron, manganese, selenium, and zinc in an animal model of alcoholic cardiomyopathy.

Alcoholic cardiomyopathy (AC) is one of the diseases caused by alcohol abuse, and there has been considerable debate about the possibility that nutritional factors may be important in the etiology of AC. In addition, there is evidence that ethanol may affect the metabolism of trace elements. The purpose of this investigation was to determine if chronic ethanol administration produces changes in the metabolism of the essential metals copper, iron, manganese, zinc, and selenium using an animal model of AC. Eighteen male Sprague-Dawley rats were divided into three groups: an ad libitum control group (AL), a pair-fed control group (PF), and an ethanol-dosed group (ETOH). The latter group received gradually increasing concentrations (5-25%) of ethanol in the drinking water for 15 wk. Food intake was monitored and urine and feces collected for a 4-d period during the study to determine ethanol effects on trace-element balance. Growth of both the PF and ETOH animals was inhibited. Ethanol produced substantial increases in liver manganese and decreases in liver copper and zinc. Metal concentrations in heart and concentrations in other tissues studied (spleen, testes, brain, bone, kidney, and muscle) did not differ significantly among the groups, except for testes selenium and kidney zinc. Reduced food intake and ethanol ingestion were associated with a reduced percentage of ingested selenium excreted in the urine. Deficiencies of copper, iron, manganese, selenium, and zinc in myocardial tissue are not likely to be involved in the pathogenesis of AC in the rat.