Abstract

Deltamethrin is a widely used pyrethroid insecticide that can induce renal toxicity through oxidative stress, leading to structural and functional damage to the kidneys. α-tocopherol (Vitamin E), a potent antioxidant, may protect against deltamethrin-induced nephrotoxicity by scavenging free radicals and preserving renal tissue integrity. This study evaluated the protective efficacy of α-tocopherol against renal toxicity induced by deltamethrin exposure in adult male Wistar rats. The study lasted for thirty-five (35) days. We selected 40 male rats and assigned them to 8 groups (n=5). Group A was control, group B received deltamethrin 25 mg/kg bw/day only, C received deltamethrin only 12.5 mg/kg bw/day only, D received deltamethrin only 6.25 mg/kg bw/day only, E received 100mg/kg/bw/day α-tocopherol only, F received 100mg/kg/bw/day α-tocopherol + 25 mg/kg bw/day deltamethrin, G received 100mg/kg/bw/day α-tocopherol + 12.5 mg/kg bw/day deltamethrin and H received 100mg/kg/bw/day α-tocopherol + 6.25 mg/kg bw/day deltamethrin. At the end of the treatment period, blood samples were collected for analysis. Total protein was analyzed using the spectrophotometric methods of Biuret, Bradford, and erythrosine–b; albumin was estimated; creatinine and urea were measured using enzymatic methods. Histological sections of the kidney were mounted on slides, stained with hematoxylin and eosin (H&E). Photomicrographs were generated. Results show a dose-dependent significant (p=0.05) increase in Albumin, Urea, Total protein, and creatinine levels in groups B, C, and D compared to other groups co-administered α-tocopherol. Histopathological examination of deltamethrin-only groups revealed marked glomerular distortion, tubular cast formation, and epithelial deformation driven by severe oxidative stress. In contrast, co-treatment with α-tocopherol preserved renal architecture, maintaining intact glomeruli and preventing tubular necrosis. In conclusion, deltamethrin induces dose-dependent nephrotoxicity while α-tocopherol confers substantial protection against these adverse effects, suggesting that α-tocopherol may serve as a beneficial therapeutic agent in attenuating pesticide-induced renal injury.