Exploring Nanosilver-Induced Cytotoxicity in Renal Tissues

This study examined the nephrotoxic effects of silver nanoparticles (AgNPs) in Wistar rats over 90 days. A total of 35 rats were divided into control (20 rats) and AgNPs-treated (15 rats) groups. The treated group received AgNPs orally at 30 mg/kg body weight daily. Serum biochemical analysis showed a significant increase in creatinine, urea, uric acid, and potassium levels in treated rats, indicating impaired kidney function. Oxidative stress markers, such as increased TBARS levels and reduced CUPRAC antioxidant activity, were observed in kidney tissues. Apoptosis percentage was significantly higher in treated rats at 30, 60, and 90 days, suggesting caspase pathway activation. Urinary analysis revealed progressive proteinuria. Histopathological examination of treated rats showed glomerular congestion, Bowman's capsule damage, tubular necrosis, and interstitial hemorrhages. Immunoperoxidase staining confirmed immune complex deposition in the glomeruli, indicating immune-mediated glomerulonephritis. These findings suggest that prolonged exposure to AgNPs at 30 mg/kg is nephrotoxic, leading to kidney dysfunction, oxidative stress, apoptosis, and immune-mediated kidney damage.