Redox‐Associated Renal and Male Reproductive Alterations Following Dexamethasone Exposure in Male Rats: Histopathological and Spermatological Evaluations

Dexamethasone (DEX) is widely used in clinical practice, although it may also cause oxidative stress-related damage in different tissues, including the kidney and male reproductive system. This study investigated DEX-induced renal and reproductive injury in rats and evaluated the modulatory effect of reduced glutathione on DEX-associated redox imbalance and tissue injury. Thirty-five adult male Wistar rats were divided into five groups (n = 7): control, DEX (7 mg/kg/day, intraperitoneally, for 7 days), GSH (0.2 g/kg/day, oral gavage, for 7 days), co-administration (DEX + GSH for 7 days; DG7), and extended treatment (DEX + GSH for 7 days followed by seven additional days of GSH; DG14). Spermatological parameters, chlortetracycline-based capacitation status, total antioxidant status (TAS) and total oxidant status (TOS) in epididymal sperm samples, and histopathological changes in the kidney, testis, and epididymis were evaluated. DEX impaired sperm motility, concentration, and capacitation, decreased TAS, increased TOS, and caused marked renal and testicular histopathological alterations, including increased collagen deposition, disruption of seminiferous tubule architecture, and reduced spermatogenic activity. GSH attenuated these changes, and the DG14 regimen was associated with the most evident overall improvement. These findings suggest that DEX exposure was associated with redox imbalance and renal and male reproductive alterations, while prolonged GSH administration may modulate glutathione sensitive redox changes related to DEX-induced tissue injury.