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甲基汞会损害早期发育中的运动功能,并诱导小脑颗粒细胞发生氧化应激。

Methylmercury impairs motor function in early development and induces oxidative stress in cerebellar granule cells.

机构信息

Department of Biology, Washington College, 300 Washington Avenue, Chestertown, MD 21620, USA.

出版信息

Toxicol Lett. 2013 Oct 9;222(3):265-72. doi: 10.1016/j.toxlet.2013.08.002. Epub 2013 Aug 12.

Abstract

Environmental toxicants such as methylmercury play a critical role in the pathogenesis of many neurodevelopmental disorders. Environmental exposure to methylmercury frequently occurs at low doses, most frequently through fish consumption. Although the general population is at risk for exposure, pregnant women and young children are the most vulnerable. A common symptom of perinatal exposure to methylmercury is increased sensory (visual) deficits, motor impairment, and an overall cognitive decline. Research has indicated that the developing cerebellum, specifically the cerebellar granular layer, is particularly vulnerable to methylmercury neurotoxicity. This review examines the effects of low-level methylmercury exposure on motor coordination. We specifically focus on the role of cerebellar granule cells in methylmercury neurotoxicity. We suggest that methylmercury induces oxidative stress in cerebellar granule cells, which subsequently results in apoptotic cell death. Understanding the mechanism by which methylmercury induces toxicity within the developing brain will allow for enhanced treatments and potential reversal of the detrimental effects.

摘要

环境毒素,如甲基汞,在许多神经发育障碍的发病机制中起着关键作用。环境中甲基汞的暴露通常发生在低剂量下,最常见的途径是通过鱼类摄入。尽管一般人群都有暴露的风险,但孕妇和幼儿是最脆弱的。围产期接触甲基汞的一个常见症状是感觉(视觉)缺陷增加、运动障碍和整体认知能力下降。研究表明,发育中的小脑,特别是小脑颗粒层,对甲基汞的神经毒性特别敏感。这篇综述考察了低水平甲基汞暴露对运动协调的影响。我们特别关注小脑颗粒细胞在甲基汞神经毒性中的作用。我们认为,甲基汞在小脑颗粒细胞中诱导氧化应激,随后导致细胞凋亡。了解甲基汞在发育中的大脑中引起毒性的机制将有助于增强治疗效果,并有可能逆转其有害影响。

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