张泓, 刘建文, 颜崇淮. 二十二碳六烯酸(DHA)对甲基汞神经毒性的保护效应及机制研究进展[J]. 环境与职业医学, 2020, 37(2): 187-191. DOI: 10.13213/j.cnki.jeom.2020.19577
引用本文: 张泓, 刘建文, 颜崇淮. 二十二碳六烯酸(DHA)对甲基汞神经毒性的保护效应及机制研究进展[J]. 环境与职业医学, 2020, 37(2): 187-191. DOI: 10.13213/j.cnki.jeom.2020.19577
ZHANG Hong, LIU Jian-wen, YAN Chong-huai. Research progress on protective effects and mechanisms of docosahexaenoic acid (DHA) on neurotoxicity induced by methylmercury[J]. Journal of Environmental and Occupational Medicine, 2020, 37(2): 187-191. DOI: 10.13213/j.cnki.jeom.2020.19577
Citation: ZHANG Hong, LIU Jian-wen, YAN Chong-huai. Research progress on protective effects and mechanisms of docosahexaenoic acid (DHA) on neurotoxicity induced by methylmercury[J]. Journal of Environmental and Occupational Medicine, 2020, 37(2): 187-191. DOI: 10.13213/j.cnki.jeom.2020.19577

二十二碳六烯酸(DHA)对甲基汞神经毒性的保护效应及机制研究进展

Research progress on protective effects and mechanisms of docosahexaenoic acid (DHA) on neurotoxicity induced by methylmercury

  • 摘要:

    甲基汞是一种具有神经毒性的环境污染物,会对人体中枢神经系统造成不可逆的损害。二十二碳六烯酸(DHA)是一种n-3长链多不饱和脂肪酸,是神经细胞生长过程中的重要成分。许多研究发现,DHA可对甲基汞导致神经系统损害产生潜在的保护作用,但机制尚不清楚。本文首先介绍了甲基汞的神经毒理作用机制,明确了甲基汞对人体的神经损伤作用。其次介绍了DHA对甲基汞暴露潜在的神经保护机制,包括DHA可通过增强细胞抗氧化能力,降低细胞对甲基汞的吸收,平衡细胞内外钙离子水平,改变细胞骨架等机制对暴露于甲基汞的细胞产生保护作用。在发育的关键时期应减少或避免甲基汞暴露,增加DHA的摄入,以保障神经系统的正常发育。最后,本文提出未来应关注多不饱和脂肪酸对甲基汞神经毒性的作用及其机制,为甲基汞所致神经损害的保护探讨新的方向。

     

    Abstract:

    Methylmercury is a neurotoxic environmental pollutant which can cause irreversible damage to the central nervous system. Docosahexaenoic acid (DHA) is an n-3 polyunsaturated fatty acid, an important component for the growth of nerve cells. Many studies have found that DHA can protect against neuronal damage caused by methylmercury, but the mechanism is still not clear. Firstly, this paper introduced the neurotoxicological mechanism of methylmercury and clarified the neurological damage of methylmercury on humans. Secondly, this paper introduced proposed potential mechanism of DHA on methylmercury-induced neurotoxicity, and concluded that DHA can protect neurons through enhancing cell antioxidant capacity, reducing the absorption of methylmercury by cells, balancing intracellular and extracellular calcium levels, and changing cytoskeleton. Therefore, methylmercury exposure should be avoided during critical periods of development, and DHA supplementation may assist normal development of the nervous system. Finally, this paper proposed that we should pay attention to the effects of polyunsaturated fatty acids on methylmercury neurotoxicology and underlying mechanisms, and explore a new direction for studies on the protection of neuronal damage caused by methylmercury.

     

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