Effect of Curcumin on Aflatoxin B1–Induced Toxicity in Rats: A Biochemical and Histopathological Study

Abstract

Objective: The aim of the present study was to investigate the protective effect of curcumin against aflatoxinB1 (AFB1) induced hepatotoxicity. Materials and Methods: Twenty-eight healthy adult male Wistar rats were divided into four groups. Rats of the first group received basal diet and served as control. Rats in the second group received curcumin orally (15mg/5ml/kg body weight) whereas, rats in the third groups injected with single intraperitoneal injection of AFB1 (3mg/kg BW). Rats in the fourth group received a combination of second and third groups for five weeks. Results: Biochemical analysis of serum samples indicated a significant increase in aspartate transaminase (AST) and alanine transaminase (ALT) activities and total cholesterol and creatinine concentrations along with significant decrease in protein content of AFB1 intoxicated rats compared to control group. Oral administration of curcumin along with injected AFB1 restored AST, ALT, total cholesterol, creatinine and total protein near to control values. Biochemical analysis of liver antioxidants revealed a significant (P < 0.05) reduction in catalase (CAT) and superoxide dismutase (SOD) activities and hepatic reduced glutathione (GSH) content in rats injected with AFB1 compared to control. On the contrary, oral administration of curcumin along with injected AFB1 enhanced hepatic CAT and SOD activities and GSH concentration towards the control values, suggesting that curcumin could improve the antioxidant status in AFB1 induced oxidative stress. The Biochemical findings were supported by histopathology of liver tissues which indicated vacuolar degeneration and necrotizing changes in liver of rats intoxicated with AFB1 and significant amelioration of these effects in these rats whenever treated with curcumin. Conclusion: Conclusively, oral administration of curcumin along with AFB1 caused significant inhibition in AFB1-induced hepatotoxicity in rats by increasing the concentration of GSH and activation of antioxidant enzymes.