The present study was undertaken to evaluate methylmercury-induced alterations in hepatic enzymes and oxidative stress markers in liver tissue of rainbow trout (Oncorhynchus mykiss) by using a perfusion method, and to explore possible protective effect of vitamin C against these alterations. Forty-eight fish were divided into six groups containing control, test, and amelioration groups. The liver of fish in the test groups were exposed to different doses of methylmercury, i.e., 0.6, 1.2, and 2.4 μg L−1, respectively, for 120 min. In the amelioration group, liver was treated with vitamin C (17.2 μg L−1) along with high dose (2.4 μg L−1) of methylmercury. The results of the present study showed that exposure with 0.6, 1.2, and 2.4 μg L−1 of methylmercury significantly increased (p < 0.05) hepatic enzyme activities (alanine transaminase (ALT), aspartate transaminase (AST), and Lactate dehydrogenase (LDH)) and malondialdehyde (MDA) level, as a marker of lipid peroxidation. On the other hand, the concentration of reduced glutathione (GSH) and total antioxidant capacity of the liver decreased (p < 0.05) in the methylmercury-exposed groups when compared to the control group. Pearson’s correlation analysis revealed a positive correlation between MDA concentration and ALT, AST, and LDH activities in the methylmercury groups, suggesting that the enhanced lipid peroxidation may be linked to hepatic damage caused by methylmercury. Treatment with vitamin C in methylmercury-exposed group led to a significant decrease (p < 0.05) in MDA concentration and hepatic enzyme activities and significant increase (p < 0.05) in levels of GSH and total antioxidant capacity. The values of measured parameters in the methylmercury + vitamin C group were comparable to those of the control group. The results of the present study demonstrated that methylmercury exposure induces oxidative stress in the liver of rainbow trout and treatment with vitamin C can protect fish liver against this oxidative insult.

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