In adults, a possible effect of alcohol exposure during spermatozoa production on semen parameters has been assessed in a limited number of studies with conflicting results: some indicate a detrimental effect, but other point toward no or even a protective effect of moderate amounts of alcohol [42]. Whether maternal alcohol consumption during pregnancy is associated with poor semen quality in the male offspring has, to the best of our knowledge, never been examined and published. If such an association exists it may well be a candidate cause of the large differences in semen quality between different populations and time periods [43]. In fact, moderate prenatal exposure to alcohol was associated with lower sperm concentration, and sons exposed to >4.5 drinks/week in uterus had approximately one third lower sperm concentration than sons exposed to 1 drink/week.

An ethanol-induced oxidative stress is not restricted to the liver, where ethanol is actively oxidized, but can affect various extrahepatic tissues as shown by experimental data obtained in the rat during acute or chronic ethanol intoxication. Most of these data concern the central nervous system, the heart, and the testes [44] .

That alcohol abuse may lead to testicular lipid peroxidation is suggested by the fact that ethanol is a known testicular toxin and its chronic use leads to both endocrine and reproductive failure. Because testicular membranes are rich in polyenoic fatty acids that are prone to undergo peroxidative decomposition, it is reasonable to consider that lipid peroxidation may contribute to the membrane injury and gonadal dysfunction that occurs as a result of alcohol abuse and/or chronic use. Consistent with such a mechanism for putative alcohol-associated testicular toxicity are the observed reductions in the testicular content of polyenoic fatty acids and GSH content of the testes of alcohol-fed animals as compared to isocalorically fed controls [45],

The increased conversion of xanthine dehydrogenase into xanthine oxidase as well as the activation of peroxisomal acyl CoA-oxidase linked to ethanol administration could contribute to the oxidative stress. Chronic ethanol administration elicits in the testes an enhancement in mitochondrial lipid peroxidation and a decrease in the GSH level, which appear to be correlated to the gross testicular atrophy observed. It is well known that peroxidation injury can be attenuated when it occurs in association with dietary vitamin A supplementation. Thus, it is of interest to note that vitamin A, acting as an antioxidant, stabilizes testicular membranes by reducing lipid peroxidation and prevents the alcohol-induced atrophy that occurs in animals not receiving vitamin A-enriched diets. Vitamin A supplementation attenuates the changes in lipid peroxidation, glutathione, and testicular morphology [46].

Taken together, these observations suggest that the enhanced peroxidation of testicular lipids that occurs following ethanol exposure may be an important factor in the pathogenesis of alcohol-associated gonadal injury.

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