Abstract

This study evaluates the nephroprotective effect of a copper (II)-albumin complex against bromobenzene (BB)-induced renal toxicity in male rats. BB (300 mg/kg twice weekly for 4 weeks) induced significant nephrotoxicity, evidenced by elevated serum creatinine (p< 0.01) and urea (p<0.001) versus controls. Histopathology revealed tubular necrosis and fibrosis. Co-treatment with the copper-albumin complex (400 mg/kg) reversed creatinine (p<0.05) and UA (p<0.05), demonstrating partial but significant recovery. This is the first report highlighting albumin’s dual role in enhancing copper bioavailability and renal protection. Animals (n=15/group) were divided into control, BB-only, and BB + copper-albumin groups. Serum biomarkers (urea, creatinine, and uric acid) and blinded histopathology (H&E, Sirius Red) were analyzed. The copper-albumin dose was selected based on prior efficacy studies without hepatotoxicity. Results confirm the complex’s therapeutic potential against BB-induced injury, likely via antioxidant mechanisms. The study aligns BB’s dosing with subacute toxicity models, emphasizing industrial relevance without overstating human exposure risks. In conclusion, the copper-albumin complex mitigates BB nephrotoxicity, underscoring its promise as a therapeutic agent. Further research is needed to elucidate molecular pathways and validate findings across sexes.