Environmental pollutants like methylmercury (MeHg) can bring devastating neurotoxicity to animals and human beings. Gut microbiota has been found to demethylate MeHg and promote the excretion of Hg through feces. However, the impacts of MeHg on gut microbiota and metabolites related to gut-brain interactions were less studied in mammals. The object of this study was to investigate the impacts of acute MeHg exposure on gut microbiome and metabolites together with its impact on gut integrity and related biological responses in rats. Rats were exposed to MeHg through oral administration and were sacrificed after 24 h 16 S rRNA gene sequencing was used to study the perturbance to gut microbiome and liquid chromatography mass spectrometry (LC-MS) was used for metabolomics profiling. It was found that gut was one of the target tissues of MeHg. MeHg induce the changes of intestinal microbial community structure and induce the regulating neuron activity change of intestinal neurotransmitters and metabolites on intestinal neurotransmitters and metabolites regulating the neuron activity. This was supported by the increased BDNF level. These findings may suggest a potential new mechanism regarding the neurotoxicity of MeHg. The protocols used in this study may also be applied to understand the neurotoxicity of other environmental neurotoxins like Pb, Mn, polychlorinated biphenyls, and pesticides, etc and to screen the neurotoxicity of emerging environmental contaminants.

中文翻译：

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急性口服甲基汞暴露会扰乱肠道微生物组并改变大鼠肠脑轴相关代谢产物。

甲基汞（MeHg）等环境污染物会给动物和人类带来毁灭性的神经毒性。已发现肠道菌群可使MeHg脱甲基并促进Hg通过粪便排泄。然而，在哺乳动物中，甲基汞对肠道菌群和与肠脑相互作用有关的代谢产物的影响较少。这项研究的目的是调查急性甲基汞暴露对肠道微生物组和代谢产物的影响，以及对大鼠肠道完整性和相关生物学反应的影响。大鼠通过口服暴露于MeHg中，并在24小时后处死。16 S rRNA基因测序用于研究对肠道微生物组的干扰，液相色谱质谱（LC-MS）用于代谢组学分析。发现肠是MeHg的靶组织之一。MeHg引起肠道微生物群落结构的改变，并引起肠道神经递质和代谢产物的调节神经元活性变化，而肠道神经递质和代谢产物则调节神经元活性。BDNF水平升高支持了这一点。这些发现可能暗示了有关MeHg神经毒性的潜在新机制。本研究中使用的协议还可用于了解其他环境神经毒素（如Pb，Mn，多氯联苯和杀虫剂等）的神经毒性，并筛选新兴环境污染物的神经毒性。