| This study was designed to assess the ameliorative role of vitamin E on sperm parameters, reducing male fertility due to oxidative stress induced by atenolol in adult male rats. Thirty-two adult male rats were divided into four equal groups (C, T1, T2 and T3). Where, group C (control group), group T1 treated orally with atenolol, group T2 given atenolol plus vitamin E orally, group T3 given only vitamin E orally. Heart blood was collected at zero and 56 days. Following parameters were studied: Total cholesterol concentration, peroxy nitrate concentration and reduced glutathione (GSH) concentration. Histopathological examination of testes and epididymis, Sperm viability, gonadosomatic index (GSI) and sperm DNA damage were done at 56 day.Results; results showed a significant elevation in serum total cholesterol and peroxy nitrate in group (T1), while these levels beginning to lowering significantly in group (T2). A significant (P<0.05) decreasing in (GSH) concentration with a significant (P<0.05) increasing to peroxy nitrate in group (T1) as compared with group (T2) which showed a significant (P<0.05) increasing in levels of (GSH). Histopathologically, atenolol affects the testes and epididymis by causing edema in the interstitial tissue with atrophy of leydig cells, incomplete spermatogenesis as comparing to group (T2) which showed complete spermatogenes process and sperm in the lumen of seminiferous tubules. Sperm DNA damage analysis of group (T1) showed marked induction of chromosomal damage as compared with vitamin E that ameliorates these harmful effects. In conclusion, vitamin E is a powerful antioxidant that ameliorates the deleterious effects on male reproductive system in patient treated with atenolol.
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