Biodegradable metals, such as mercury, accumulate in living organisms throughout their lives (bioaccumulation) and also in food webs (biomagnification), and can reach high concentrations in humans. Human contamination by mercury found in drinking water and food can be common, especially in riverine communities that depend on fish as their main source of protein. In vitro studies with human cell lines exposed to methylmercury showed that prolactin has cytoprotective properties against cytotoxic and mutagenic effects of this metal, and can act as a co-mitogenic factor and apoptosis inhibitor. The present study investigated, in vivo, the protective potential of prolactin against the toxic effects of methylmercury in mammals, using the mouse (Mus musculus) as a model. Biomarkers of genotoxicity (comet assay and micronucleus test) and oxidative stress (lipid peroxidation and activity of CAT and SOD enzymes), together with histological (in liver, kidney and brain tissue samples) and biochemical (renal and hepatic and measurement of Hg and PRL in the blood), were used to verify the protective potential of prolactin in mice exposed to methylmercury. It was observed, in a more expressive way, a reduction in the alterations of the renal and hepatic biochemical parameters and of the mutagenic effects in the presence of prolactin, in comparison with the isolated effects of the metal. When prolactin was used together with the metal, a decrease in histological damage and an increase in SOD enzyme activity were also observed. The study results indicate that prolactin has protective effects against toxic impacts of methylmercury.
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