testicular dysfunction

Oxidative stress plays a crucial role in the pathophysiology of reproductive and thyroid dysfunction [17, 18]. Therefore, the regimen that can alleviate oxidative stress is a promising strategy for prevention of sexual and thyroid disorders. The current investigation outlines the ameliorative effects of Vitis vinifera seed extract on dexamethasone-induced testicular and thyroid dysfunction in male albino rats.

Dexamethasone administration led to a significant decrease in body weight gain and testis weight compared with normal control group, which were in line with the findings of AL-Saeed [19] and Khorsandi [20] who demonstrated a decrease in testicular weight in dexamethasone-induced testicular toxicity in mice.  This significant reduction in the body weight gain after dexamethasone administration could be as a result of some metabolic disorders (e,g, proteolysis in muscle, loss of appetite, and increased metabolic catabolism) [21, 22]. Regarding, a significant reduction in weight of testes could be due to a decrease in seminiferous tubule size and spermatogenic arrest after dexamethasone administration [20]. Administration of grape seed extract restored the body weight gain and weights of testes in dexamethasone-intoxicated rats. The alleviation of body weight gain decline by the administration of GSE suggested that the GSE could possess some protective ingredients that prevented the loss of body weight in DEX-treated rats. Accordingly, the significant increase in the testis weights of DEX-induced rats that were treated with GSE may be attributed to the antioxidant effects of GSE that prevents cellular damage occurring as a result of oxidative stress in spermatogenic cells of the seminiferous tubules and Leydig cells of the testes [23]. This attribution was supported by the results of the current investigation which proved by the improvement in the testicular antioxidant defense markers. In the present investigation, the DEX-induced rats caused a decline in the testosterone level and these results were in harmony with previous reports for dexamethasone-induced animals [24-26].

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DEX-induced rats caused testicular dysfunction, leading to the dramatic changes in the testicular histological architecture and a significant decrease in testosterone level could be mainly as a result of inhibition of gonadotropin secretion, excessive oxidative stress and the degeneration of Leydig cells [27-29]. 


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