Toxicity of methylmercury (MeHg) to wildlife and humans results from its binding to cysteine residues of proteins, forming MeHg-cysteinate (MeHgCys) complexes that hinder biological functions. MeHgCys complexes can be detoxified in vivo, yet how this occurs is unknown. We report that MeHgCys complexes are transformed into selenocysteinate [Hg(Sec)₄] complexes in multiple animals from two phyla (a waterbird, freshwater fish, and earthworms) sampled in different geographical areas and contaminated by different Hg sources. In addition, high energy-resolution X-ray absorption spectroscopy (HR-XANES) and chromatography-inductively coupled plasma mass spectrometry of the waterbird liver support the binding of Hg(Sec)₄ to selenoprotein P and biomineralization of Hg(Sec)₄ to chemically inert nanoparticulate mercury selenide (HgSe). The results provide a foundation for understanding mercury detoxification in higher organisms and suggest that the identified MeHgCys to Hg(Sec)₄ demethylation pathway is common in nature.

中文翻译：

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鸟类，鱼类和Earth中甲基汞的去甲基化

甲基汞（MeHg）对野生生物和人类的毒性是由于其与蛋白质的半胱氨酸残基结合而形成的MeHg-半胱氨酸（MeHgCys）复合物，阻碍了生物学功能。MeHgCys复合物可以在体内排毒，但如何发生尚不清楚。我们报告说MeHgCys复合物被转换成硒代半胱氨酸[Hg（Sec）₄ ]在来自不同地理区域并受不同汞源污染的两个门（水鸟，淡水鱼和earth）的多种动物中转化为硒代半胱氨酸[Hg（Sec）₄ ]。此外，水鸟肝的高能量分辨率X射线吸收光谱（HR-XANES）和色谱-电感耦合等离子体质谱法支持Hg（Sec）₄的结合硒蛋白P和Hg（Sec）_4的生物矿化以化学惰性纳米硒化汞（HgSe）。该结果为理解高等生物中的汞排毒提供了基础，并表明已鉴定出的MeHgCys至Hg（Sec）₄脱甲基途径在自然界中很常见。