The potential effect of berberine in mercury-induced hepatorenal toxicity in albino rats

Mercury (Hg) is the third most dangerous heavy metal after arsenic and lead. Mercury’s toxicity brings serious risks to health through negative pathological and biochemical effects. The study was designed to investigate the possible protective role of berberine (BN) in mercuric chloride (HgCl2) induced oxidative stress in hepatic and renal tissues. Adult male albino Wistar rats were exposed to mercuric chloride (HgCl2; 0.4 mg/kg bwt) for 7 days. Treatment with HgCl2 induced oxidative stress by increasing lipid peroxidation and nitric oxide production along with a concomitant decrease in glutathione and various antioxidant enzymes, namely superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. HgCl2 intoxication increased the activities of liver enzymes and the bilirubin level, in addition to the levels of urea and creatinine in serum. BN (100 mg/kg bwt) treatment inhibited lipid peroxidation and nitric oxide production, whereas it increased glutathione content. Activities of antioxidants enzymes, superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, were also restored concomitantly when compared to control after BN administration. BN also inhibited the apoptotic effect of HgCl2 by increasing the expression of Bcl-2 protein in liver and kidney. Histopathological examination of the liver and kidney tissues proved the protective effect of BN against HgCl2 toxicity. These results demonstrated that BN augments antioxidant defense against HgCl2-induced toxicity and provides evidence that it has therapeutic potential as hepato- and reno-protective agent.