Ethanol is a testicular toxin and it causes fertility abnormalities with low sperm count and impaired sperm motility in men. The present study was designed to investigate plasma testosterone level and hypothalamic pituitary gonadal (HPG) axis function in alcoholic men and also effect of ethanol on systemic oxidative stress. Forty six male alcohol abusers in the age group 20-40 years were selected. Fifty five, males in the same age group served as control. Alcohol abusers had significantly low plasma testosterone with low luteinizing hormone and follicle stimulating hormone. In addition they had significantly high thiobarbituric acid reactive substances (TBARS), superoxide dismutase and glutathione S-transferase, and low glutathione, ascorbic acid, catalase, glutathione reductase and glutathione peroxidase. Moreover, serum testosterone level in alcoholics negatively correlated with duration of alcohol abuse, and TBARS. Duration dependent decreased serum testosterone level in alcohol abusers might be due to 1) increased oxidative stress which can damage Leydig and supporting Sertoli cells and 2) impaired HPG axis.
Infertility is well-established harmful effect in chronic alcoholism and so far, there is no effective treatment for this condition. The study was conducted to determine the effects of alpha tocopherol on ethanol induced testicular injuries in male albino rats of Wistar strain. Five groups (n=6) of animals were used. Group I served as control. Group II received daily 1.6g ethanol/kg body weight/day for 4 weeks orally. Group III received 1.6g ethanol+80mg alpha tocopherol/kg body weight/day for four weeks orally. Group IV received 1.6g ethanol/kg body weight for/day 4 weeks and followed by 80mg alpha tocopherol/kg body weight/day for four weeks orally. Group V received 1.6g ethanol/kg body weight/day orally for 4 weeks, followed by 4 weeks abstinence. Twently-four hours after the last treatment the rats were sacrificed using anesthetic ether. Testes were removed and used for the estimation of extent of lipid peroxidation and tissue levels of antioxidants and steroidogenic enzymes. Alpha tocopherol treatment increased the activities of testicularΔ(5), 3β-HSD. Moreover, the treatment was also associated with significant decrease in testicular oxidative stress. Ethanol-induced oxidative stress and decreased steroidogenesis can be reversed by treatment with alpha tocopherol.
To investigate reversibility of ethanol induced testicular injuries on treatment with L-ornithine-L-aspartate, male Wistar rats were treated with ethanol (1.6g/kg b.wt/day) and L-ornithine- L-aspartate (200mg/kg b.wt/ day) for 4 weeks. L-ornithine-L-aspartate effectively prevented the ethanol induced body and testes weight reduction; changes in testicular weight well correlated with body weight. Drug exhibited an ability to counteract ethanol induced oxidative challenge as it effectively reduced testicular TBARS and increased tissue ascorbic acid, GSH and activities of superoxide dismutase, catalase, GSH-Red and Se-GSH-Px. However the drug didn't show promising effect on inhibitory effect of ethanol on testicular D5, 3-beta and 17-beta HSD (hydroxy steroid dehydrogenase).
Ethanol intoxication resulted in high extent of lipid peroxidation, and reduction in antioxidant defenses (decreased GSH, GSH/GSSG ratio, and catalase, SOD and GPx activities) and (Na+/K+)-ATPase activity in kidney. Alpha-tocopherol treatment effectively protected kidney from ethanol induced oxidative challenge and improved renal (Na+/K+)-ATPase activity. Ethanol induced oxidative stress in the kidney and decreased (Na+/K+)-ATPase activity could be reversed by treatment with ascorbic acid.