Lipid peroxidation: a mechanism for ethanol-associated testicular injury in rats.

Chronic alcohol administration leads to hepatic membrane alterations which, at least in part, are due to lipid peroxidation and may contribute to the toxicity of ethanol at the level of the hepatocyte. Because changes in testicular function also occur after chronic administration of ethanol to rats, we evaluated testicular mitochondria for evidence of alcohol-associated peroxidation injury which might contribute to the gonadal injury that occurs with prolonged use of the drug. Lipid peroxidation was assessed through measurement of diene conjugates, polyenoic fatty acid composition, malonaldehyde formation, and testicular reduced glutathione levels. Compared to isocalorically matched dextrimaltose-fed controls (ISO), rats fed alcohol (ETOH) for 50 days had a decreased content of polyenoic acids and a compensatory increase in saturated fatty acids [ETOH, 50.69 +/- 0.65% (by wt); ISO, 52.93 +/- 0.72 (mean +/- SE); P less than 0.01]. This decrease in polyunsaturated fatty acid content was accompanied by an increase in diene conjugates in testicular mitochondria (ETOH, 0.455 +/- 0.053 OD units at 233 nm/mg lipid; ISO, 0.382 +/- 0.045; P less than 0.05). An increase in malonaldehyde formation also was observed in the alcohol-fed rats compared to the control level (ETOH, 21.39 +/- 1.67 nmol/mg protein; ISO, 17.50 +/- 1.39; P less than 0.05) as well as a decrease in glutathione content (ETOH, 1218 +/- 89 micrograms GSH/testes; ISO, 1638 +/- 89; P less than 0.05). Taken together, these findings support the concept that lipid peroxidation may be an important mechanism responsible, at least in part, for the toxic effect of ethanol on the testes.