Role of caftaric acid in lead-associated nephrotoxicity in rats via antidiuretic, antioxidant and anti-apoptotic activities.

Background Lead is a toxic metal that is widely distributed in the environment where caftaric acid (CA) is the ester form of caffeic acid where CA is the major dietary polyphenol present in various foods and beverages. The aim of this study was to evaluate the effect of CA in lead acetate (LA)-associated nephrotoxicity through antidiuretic, antioxidant and anti-apoptotic activities. Methods Forty-eight male albino rats divided into six equal groups; group 1 control injected intraperitoneally (ip) with saline (1 mL/kg of bw) over two weeks period, group 2 injected ip with CA (80 mg/kg of bw) over two weeks period, groups 3, 4, 5 and 6 injected ip with 100 μmol/kg of bw LA over two weeks period where groups 4, 5 & 6 co-injected ip with 1-deamino-8-D-arginine vasopressin (dDAVP) drug (1 mg/kg of bw), CA (40 mg/kg of bw), and CA (80 mg/kg of bw), respectively. Results The results obtained revealed that LA induced a significant decrease in kidney weight and serum sodium, potassium and chloride, but caused a significant increase in urinary volume, urinary excretion of sodium, potassium and chloride, serum urea, creatinine and uric acid. The LA also caused a significant decrease in kidney superoxide dismutase, glutathione peroxidase and induced a significant decrease in glutathione level while caused an increase in lipid peroxidation level. In addition, LA caused a decrease in p53 expression while induced an increase in bcl-2 expression in the kidney tissues. Co-injection of CA to LA-treated group restored all the above parameters to approach the normal values. The results supported with histopathological examinations. Conclusions In conclusion, the effect of CA on LA-related nephrotoxicity was occurred through antidiuretic, antioxidant, anti-apoptotic activities where the effect of CA was dose dependent.