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Redox-Associated Renal and Male Reproductive Alterations Following Dexamethasone Exposure in Male Rats:
Caner Öztürk1, Neşe Hayat Aksoy2, Erkan Özkan3
1Department of Reproduction and Artificial Insemination, Faculty of Veterinary Medicine, Aksaray University, Aksaray, Turkey.
Abstract:
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.
Insights
Dexamethasone (DEX) causes kidney and male reproductive injury by increasing oxidative stress. Reduced glutathione (GSH) treatment mitigated these harmful effects, with prolonged GSH showing the most benefit.
Area of Science:
- Biomedical Sciences
- Toxicology
- Reproductive Biology
Background:
- Dexamethasone (DEX) is a widely used corticosteroid with known clinical applications.
- DEX can induce oxidative stress, leading to potential damage in vital organs like the kidney and the male reproductive system.
Purpose of the Study:
- To investigate the renal and reproductive toxicity induced by Dexamethasone in a rat model.
- To evaluate the protective effects of reduced glutathione (GSH) against Dexamethasone-associated oxidative stress and tissue damage.
Main Methods:
- Adult male Wistar rats were divided into five groups: control, DEX, GSH, DEX + GSH (7 days), and DEX + GSH (14 days).
- Evaluated parameters included spermatological assessments, sperm capacitation, antioxidant/oxidant status in sperm, and histopathological examination of kidney, testis, and epididymis.
Main Results:
- DEX administration significantly impaired sperm parameters (motility, concentration, capacitation) and altered the redox balance (decreased TAS, increased TOS).
- Histopathological analysis revealed DEX-induced renal and testicular damage, characterized by collagen deposition, disrupted architecture, and reduced spermatogenesis.
- GSH treatment attenuated DEX-induced toxicity, with the extended 14-day regimen (DG14) showing the most significant improvement.
Conclusions:
- Dexamethasone exposure leads to significant renal and male reproductive system injury, primarily through redox imbalance.
- Reduced glutathione demonstrates a protective effect against DEX-induced oxidative stress and tissue damage.
- Prolonged administration of GSH may be a viable strategy to modulate glutathione-sensitive redox changes and mitigate DEX-related toxicity.
