Harmine Mitigates Liver Injury Induced by Mercuric Chloride via the Inhibition of Oxidative Stress

The mercury-induced liver pathogenesis is mainly mediated by oxidative stress. The aim of the current study was to evaluate the possible ameliorative effect of harmine, a natural compound, on liver toxicity induced by mercury chloride (HgCl2).

Forty-two male Balb/c mice were randomly divided into six groups (n = 7): Control, HgCl2 (0.5 mg/kg), harmine (20 mg/kg), and HgCl2 (0.5 mg/kg) + harmine (5, 10, or 20 mg/kg). The mice received treatments once per day for two weeks. After this period, the blood and tissue samples were collected for analyses.

HgCl2 caused a significant increase in levels of hepatic enzymes alanine aminotransferase, aspartate transaminase, and alkaline phosphatase; while harmine ameliorated these effects. Harmine in HgCl2-intoxicated mice, showed protective effects as evidenced by the increase in liver relative weight to body as well as the diameter of central vein in the co-treated group. Serum levels of malondialdehyde and nitric oxide increased in HgCl2, while they were declined in harmine co-treated groups compared to HgCl2 group. The serum level of superoxide dismutase and total antioxidant capacity improved following harmine treatment in the co-administrated group compared to HgCl2 group. Moreover, gene expression analysis demonstrated that harmine treatment improved the HgCl2-induced decreasing of Ho-1, Nrf2, Hqo1, and Trx1. The histopathological examination confirmed the protective effects of harmine.

Mercury can induce toxicity by elevation of oxidative stress in the liver and harmine attenuates hepatic injury induced by HgCl2, at least in part, through its antioxidant activities.