In Vivo Antioxidant And Kidney Protective Potential Of Atorvastatin In Rat Cadmium-Induced Toxicity

Purpose: Environmental and occupational exposure to cadmium chloride is known to cause nephrotoxicity linked with oxidative stress in humans and animals. This study used Atorvastatin to examine its effect on cadmium chloride-induced nephrotoxicity in rat model using biochemical and histological methodologies.Methods: Experiments were performed on 56 adult male Wistar rats (200 ±20 g), randomly assigned to eight groups. Atorvastatin was administered by oral for 15 days at 20 mg/kg/day, started 7 days before cadmium chloride intraperitoneal administration (1, 2, and 3 mg/kg) for eight days. On day 16, blood samples were collected, and kidneys were excised to evaluate the biochemical and histopathological changes.Cadmium chloride significantly increased malondialdehyde (MDA), serum creatinine (Cr), blood urea nitrogen (BUN), and decreased superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GPx) levels. Results: Administration of Atorvastatin (20 mg/kg) significantly improved lipid peroxidation, glutathione and activities of antioxidant enzymes and significantly decreased BUN and Creatinine. Atorvastatin clearly improved the histological changes, demonstrating its protective role against Cadmium chloride-induced kidney injury.Conclusion: Treatment with Atorvastatin significantly improves all biochemical parameters and suggests a protecting role against cadmium chloride-induced oxidative stress and histological changes in rat kidney.