Methylmercury (MeHg) remains a global public health issue because of its frequent presence in human food sources obtained from the water. The excretion of MeHg in humans occurs slowly with a biological half-time of 32–47 days. Short-term MeHg exposure may cause long-lasting neurotoxicity. The excretion through feces is a major route in the demethylation of MeHg. Accumulating evidence suggests that the intestinal microbiota plays an important role in the demethylation of MeHg, thereby protecting the host from neurotoxic effects. Here, we discuss recent developments on the role of intestinal microbiota in MeHg metabolism, based on in vitro cell culture experiments, experimental animal studies and human investigations. Demethylation by intestinal bacteria is the rate-limiting step in MeHg metabolism and elimination. The identity of bacteria strains responsible for this biotransformation is currently unknown; however, the non-homogenous distribution of intestinal microbiota may lead to different demethylation rates in the intestinal tract. The maintenance of intestinal barrier function by intestinal microbiota may afford protection against MeHg-induced neurotoxicity, which warrant future investigations. We also discuss studies investigating the effects of MeHg exposure on the population structural stability of intestinal microbiota in several host species. Although this is an emerging area in metal toxicity, current research suggests that a change in certain phyla in the intestinal microbiota may indicate MeHg overexposure.

甲基汞 (MeHg) 仍然是一个全球公共卫生问题，因为它经常存在于人类从水中获取的食物中。人体中甲基汞的排泄缓慢，生物半衰期为 32-47 天。短期接触甲基汞可能会导致长期的神经毒性。粪便排泄是甲基汞去甲基化的主要途径。越来越多的证据表明，肠道微生物群在甲基汞的去甲基化中发挥着重要作用，从而保护宿主免受神经毒性作用。在这里，我们基于体外细胞培养实验、实验动物研究和人体研究，讨论肠道微生物群在甲基汞代谢中的作用的最新进展。肠道细菌的去甲基化是甲基汞代谢和消除的限速步骤。目前尚不清楚负责这种生物转化的细菌菌株的身份。然而，肠道微生物群的非均匀分布可能导致肠道内不同的去甲基化率。肠道微生物群维持肠道屏障功能可能会提供针对甲基汞引起的神经毒性的保护，这值得未来的研究。我们还讨论了研究甲基汞暴露对几种宿主物种肠道微生物群结构稳定性影响的研究。尽管这是金属毒性的一个新兴领域，但目前的研究表明，肠道微生物群中某些门的变化可能表明甲基汞过度暴露。