The Hepatoprotective Effect of Gallic Acid on Mercuric Chloride-Induced Liver Damage in Rats

Mercury has a variety of industrial applications and is well-known for its hematotoxic, hepatotoxic, neurotoxic, nephrotoxic, and genotoxic effects.
This study was carried out to assess the protective effects of gallic acid against mercuric chloride-induced oxidative stress in albino rats.
A total of 35 male Wistar rats were divided into 5 groups (7 rats per group). Groups 1 and 2 were used as the negative and positive controls, respectively and received normal saline (2 mL/kg/day, po) and mercuric chloride (0.4 mg/kg/day, po) for 28 days. Group 3 only received gallic acid (200 mg/kg/day, po) for 28 days, whereas groups 4 and 5 received gallic acid (50 and 200 mg/kg/day, respectively) after 1 hour, followed by mercuric chloride (0.4 mg/kg/day, po) for 28 days.
The results demonstrated that treatment with gallic acid significantly diminished the mercuric chloride-induced increase in the serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and lipid peroxidation in liver tissues. In addition, gallic acid treatment increased the level of glutathione peroxidase, superoxide dismutase, and catalase activity and lowered the glutathione level in liver tissues, compared to the mercuric chloride group. The liver of rats, treated with mercuric chloride, showed degenerated cells (with mild cytoplasmic vacuolation and blebbing), binucleated cells, and significant sinusoidal dilation.
It can be concluded that gallic acid restores the activities of antioxidant enzymes and tissue markers in mercuric chloride-treated rats, probably by scavenging free radicals and improving the antioxidant defense mechanisms.