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

John Bogden, Suad Al-Rabiai, Shamshad H. Gilani

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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 animat model of AC. Eighteen mate 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.

Original languageEnglish (US)
Pages (from-to)407-417
Number of pages11
JournalJournal of Toxicology and Environmental Health
Volume14
Issue number2-3
DOIs
StatePublished - Jan 1 1984
Externally publishedYes

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Alcoholic Cardiomyopathy
Selenium
Manganese
Metabolism
Zinc
Copper
Animals
Ethanol
Iron
Animal Models
Eating
Trace Elements
Trace elements
Liver
Testis
Rats
Metals
Urine
Tissue
Kidney

All Science Journal Classification (ASJC) codes

  • Toxicology
  • Pollution

Cite this

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abstract = "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 animat model of AC. Eighteen mate 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.",
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Effect of chronic ethanol ingestion on the metabolism of copper, iron, manganese, selenium, and zinc in an animal model of alcoholic cardiomyopathy. / Bogden, John; Al-Rabiai, Suad; Gilani, Shamshad H.

In: Journal of Toxicology and Environmental Health, Vol. 14, No. 2-3, 01.01.1984, p. 407-417.

Research output: Contribution to journalArticle

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