Autism is defined by a behavioral set of stereotypic and repetitious behavioral patterns in combination with social and communication deficits. There is emerging evidence supporting the hypothesis that autism may result from a combination of genetic susceptibility and exposure to environmental toxins at critical moments in development. Mercury (Hg) is recognized as a ubiquitous environmental neurotoxin and there is mounting evidence linking it to neurodevelopmental disorders, including autism. Of course, the evidence is not derived from experimental trials with humans but rather from methods focusing on biomarkers of Hg damage, measurements of Hg exposure, epidemiological data, and animal studies. For ethical reasons, controlled Hg exposure in humans will never be conducted. Therefore, to properly evaluate the Hg-autism etiological hypothesis, it is essential to first establish the biological plausibility of the hypothesis. This review examines the plausibility of Hg as the primary etiological agent driving the cellular mechanisms by which Hg-induced neurotoxicity may result in the physiological attributes of autism. Key areas of focus include: (1) route and cellular mechanisms of Hg exposure in autism; (2) current research and examples of possible genetic variables that are linked to both Hg sensitivity and autism; (3) the role Hg may play as an environmental toxin fueling the oxidative stress found in autism; (4) role of mitochondrial dysfunction; and (5) possible role of Hg in abnormal neuroexcitory and excitotoxity that may play a role in the immune dysregulation found in autism. Future research directions that would assist in addressing the gaps in our knowledge are proposed.

中文翻译：

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汞在自闭症病因学中的作用的合理性：细胞视角


自闭症的定义是一系列刻板和重复的行为模式以及社交和沟通缺陷。越来越多的证据支持这样的假设：自闭症可能是遗传易感性和发育关键时刻接触环境毒素共同导致的。汞 (Hg) 被认为是一种普遍存在的环境神经毒素，越来越多的证据表明它与神经发育障碍（包括自闭症）有关。当然，证据并非来自人体实验，而是来自于汞损伤生物标志物、汞暴露测量、流行病学数据和动物研究的方法。出于道德原因，永远不会对人类进行受控汞暴露。因此，为了正确评估Hg-自闭症病因学假说，首先必须确定该假说的生物学合理性。本综述探讨了汞作为驱动细胞机制的主要病因的合理性，汞诱导的神经毒性可能通过该机制导致自闭症的生理特征。重点关注领域包括：（1）自闭症汞暴露途径和细胞机制； (2) 与汞敏感性和自闭症相关的可能遗传变量的当前研究和实例； (3) 汞可能作为一种环境毒素，加剧自闭症中的氧化应激； (4)线粒体功能障碍的作用； (5)汞在异常神经兴奋和兴奋性毒性中的可能作用，这可能在自闭症中发现的免疫失调中发挥作用。提出了有助于解决我们知识空白的未来研究方向。