| Summary: | Cadmium contributes to nephrotoxicity linked with oxidative stress in humans and animals. This study used Atorvastatin to examine its effect on cadmium chloride-induced nephrotoxicity in a rat model using biochemical and histological methodologies. Experiments were performed on 56 adult male Wistar rats (200 ± 20 g), randomly assigned to eight groups. Rats in Group A received physiologic saline. Group B was treated with a dosage of 20 mg/ kg body weight/day AT for 15 days. Groups C, D, and E received CdCl2 with dosages of 1, 2, and 3 mg/kg body weight, respectively. Groups F, G, and H were pretreated with Atorvastatin, 30 min prior to the administration of CdCl2. Rats received intra-gastric Atorvastatin for 15 days during which cadmium chloride was given from days 8 to 15. 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. Administration of Atorvastatin (20 mg/kg) significantly decreased lipid peroxidation, BUN and Cr, while it significantly increased glutathione and antioxidant enzymes activity. Atorvastatin improved the histological changes and all biochemical markers and shed light on its protecting role against cadmium chloride-induced oxidative stress in the kidney.
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