Abstract
The hypothesis is presented that lipid peroxidation is responsible for the damage in skeletal and cardiac muscle of chronic alcoholic subjects. The enhanced lipid peroxidation is caused by the accumulation of oxygen radicals. Both excessive production and decreased disposal of oxygen radicals can arise from the acetaldehyde formed in the oxidation of ethanol. Although acetaldehyde from hepatic sources may contribute, muscle itself can generate significant amounts of acetaldehyde through the action of muscle catalase. The effects of alcohol on other tissues, and its known longterm effects on membranes lend support to this hypothesis. The ultrastructural features of the alcoholic myopathies provide further support. The resemblance between vitamin E-deficiency myopathy and the alcoholic myopathies is strong additional evidence in favor of this hypothesis.
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