VITAMIN A AT PHARMACOLOGIC DOSES AMELIORATES THE MEMBRANE LIPID PEROXIDATION INJURY AND TESTICULAR ATROPHY THAT OCCURS WITH CHRONIC ALCOHOL FEEDING IN RATS

The interaction of ethanol (ETOH) with testicular subcellularmembranes contributes, at least in part, to alcohol-inducedgonadal dysfunction. Vitamin A reaches the testes via the circulationas the retinyl ester and is converted to the free alcohol (retinol)and then to the aldehyde (retinal); retinal is the form of thevitamin which is essential for normal spermato-genesis. Becauseretinol can function as a free radical scavenger, testicularmitochondria were evaluated for evidence of a protective roleprovided by supplemental dietary vitamin A on ETOH-induced alterationsin testicular structure and function in rats. Lipid peroxidationwas evaluated by measurement of malonaldehyde formation andglutathione content of the testes. Compared to isocaloricallymatched dextrimaltose-fed controls (ISO) receiving a modifiedvitamin A containing diet, rats fed the corresponding ETOH dietfor 50 days had a reduced testes/body ratio (ETOH: 0.0114±0.0004vs ISO: 0.0128 ±0.0004). Mitochondrial enriched extractsobtained from the testes of these ETOH-fed rats showed significantincreases in malonaldehyde formation; moreover, gluthathionelevels were reduced in the testes of the alcohol-fed animalswhen compared to their isocaloric controls. In contrast, noevidence for testicular atrophy was present in ETOH-fed ratsreceiving a standard vitamin A enriched diet; moreover, suchETOH-fed rats had a reduced rate of malonaldehyde formationas compared to their respective controls. Similarly, glutathionelevels were not depleted in the testes of the ETOH-fed ratsreceiving the vitamin A enriched diet. Taken together, thesedata suggest that lipid peroxidation is a consequence of ethanolmetabolism which can be attenuated, at least in part, by vitaminA.