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In order to develop a preventive strategy against ethanol-induced oxidative damages on various tissues and organs, we have examined the protective effect of aspartate on the pathogenesis of testes in the ethanol treated animals. Adult male Sprague-Dawley rats were given ethanol in an amount of 36% of total calories via Lieber-DeCarli liquid diet for 6 weeks without or with aspartate (2 mM in the diet). The control group was pair-fed the diet containing isocaloric dextrin-maltose instead of ethanol. The pathogenesis of testes at post- 6 weeks of experiments were carried out by histochemistry and biochemical parameters for oxidative stress such as the level of thiobarbituric acid reactive substances (TBARS) and the activities of glutathione utilizing enzymes were also examined. Chronic ethanol administration resulted in the increased amount of thiobarbituric acid reactive substances (TBARS) in the testes, which was significantly lessened by concurrent aspartate treatment (p &lt; 0.05). In addition to this, liver function test indicated by alkaline phosphatase activity in serum showed that the ethanol-induced hepatotoxicity was significantly ameliorated by aspartate administration. And the activities of glucose-6-phosphate dehydrogenase and glutathione transferase in testis cytosol were decreased in the ethanol treated rats (p &lt; 0.01 and &lt; 0.005, respectively). These data suggest that aspartate may attenuate the ethanol-induced oxidative tissue damage in rat testes possibly through a redox-related protective effect on peroxidation.

Aspartate modulates the ethanol-induced oxidative stress and glutathione utilizing enzymes in rat testes.