Intensive Swimming Exercise-Induced Oxidative Stress and Reproductive Dysfunction in Male Wistar Rats: Protective Role of α-Tocopherol Succinate

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Abstract
In the present study, 30 male rats (age 3 mos, Wt 128.6 ± 3.7 g) were randomly divided into Control group (CG), Experimental group (EG), and Supplemented group (SG), 10 per group. An exercise protocol (3 hrs swimming per day, 5 days a week for 4 weeks) was followed in EG and SG, with no exercise in CG. In SG, α-tocopherol succinate was injected subcutaneouly at a dose of 50 mg•kg−1per body weight per day. After 4 weeks of exercise, significant diminutions (p < 0.05) were noted in somatic indices of testes and accessory sex organs; seminiferous tubuler diameter (STD); testicular Δ5, 3β-hydroxysteroid dehydrogenase (Δ5, 3β-HSD) 17 β-hydroxysteroid dehydrogenase (17 β-HSD) activities; plasma levels of testosterone (T), luteinizing hormone (LH); preleptotine spermatocytes (pLSc), mid-pachytene spermatocytes (mPSc), and Stage 7 spermatids (7 Sd); testicular α-tocopherol and glutathione (GSH) content; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and glutathione-s-transferase (GST) activities in EG when compared to CG. Moreover, a significant elevation (p < 0.05) in malondialdehyde (MDA) was found in testes of EG compared to CG. No significant alteration was noted in body weight among the groups. Co-administration of α-tocopherol succinate restored the above parameters. Intensive swimming exercise-induced oxidative stress causes dysfunction in the male reproductive system, which can be protected by α-tocopherol succinate. Key words: spermatogenesis, steroidogenesis, lipid peroxidation, vitamin E