甲基汞是环境中普遍存在的神经毒性物质,和健康问题,特别是通过食用海鲜,remain.谷胱甘肽(GSH)介导的解毒和甲基汞的排泄是已知的代谢解毒途径。我们还发现了内源性超硫化物将甲基汞转化为无毒代谢物如双甲基汞硫化物的机制。然而,这些代谢物的数量很少,而甲基汞被超硫化物解毒的重要性还没有得到很好的理解。甲基汞在体内与硫醇基结合,但也可与高反应性硒醇(硒代半胱氨酸残基)反应。这种共价键(S-汞化和Se-汞化)通过与其他硫醇和硒醇的亲核取代反应而断裂,然而,超硫化物对这种取代反应的贡献尚不清楚。有趣的是,最近的一项研究表明,硒蛋白P,血浆中主要的硒转运蛋白,与甲基汞结合,然而,硒汞没有确定。在这次审查中,我们介绍了这一系列反应,并讨论了它们与超硫化物在甲基汞毒性中的作用。
Methylmercury is a ubiquitous neurotoxic substance present in the environment, and health concerns, especially through the consumption of seafood, remain. Glutathione (GSH)-mediated detoxification and the excretion of methylmercury are known metabolic detoxification pathways. We have also discovered a mechanism by which endogenous super-sulfides convert methylmercury to nontoxic metabolites such as bis-methylmercury sulfide. However, these metabolites are present in very small quantities, and the significance of the detoxification of methylmercury by super-sulfides is not well understood. Methylmercury binds to thiol groups in vivo but can also react with highly reactive selenols (selenocysteine residues). Such covalent bonds (S-mercuration and Se-mercuration) are broken by nucleophilic substitution reactions with other thiol and selenols, however, the contribution of super-sulfides to this substitution reaction is not well understood. Interestingly, a recent study suggested that selenoprotein P, the major selenium transport protein in plasma, binds to methylmercury, however, Se-mercuration was not determined. In this review, we introduce these series of reactions and discuss their involvement with super-sulfides in methylmercury toxicity.