牛侨. 探究环境因素损害神经机制,尝试预防性干预措施[J]. 环境与职业医学, 2023, 40(3): 237-238. DOI: 10.11836/JEOM22485
引用本文: 牛侨. 探究环境因素损害神经机制,尝试预防性干预措施[J]. 环境与职业医学, 2023, 40(3): 237-238. DOI: 10.11836/JEOM22485
NIU Qiao. Exploring the mechanism of neurological damage by environmental factors and targeted preventive interventions[J]. Journal of Environmental and Occupational Medicine, 2023, 40(3): 237-238. DOI: 10.11836/JEOM22485
Citation: NIU Qiao. Exploring the mechanism of neurological damage by environmental factors and targeted preventive interventions[J]. Journal of Environmental and Occupational Medicine, 2023, 40(3): 237-238. DOI: 10.11836/JEOM22485

探究环境因素损害神经机制,尝试预防性干预措施

Exploring the mechanism of neurological damage by environmental factors and targeted preventive interventions

  • 摘要:

    神经系统是人体最重要的系统,越来越多神经毒性化学物作用于神经系统,造成认知功能损害。本文对环境因素的神经毒作用及与神经退行性疾病的关系做了扼要介绍。针对常见的金属铝、锰、铁对神经系统的损害,本专栏尝试了较为客观的影像学指标和认知量表相结合评价损害程度,用体外实验探讨了毒作用机制,包括调控多巴胺神经递质分泌、tau蛋白过度磷酸化。专栏文章还针对电离辐射对神经系统的损害,尝试用富氢水干预并阐述了干预机制是调控磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)/半胱氨酸天冬氨酸特异性蛋白酶9(Caspase-9)通路、Toll样受体4(TLR4)/核因子-κB(NF-κB)信号通路。

     

    Abstract:

    Nervous system is the most important system of human body. More and more neurotoxic chemicals are found to inflict effects on nervous system, causing cognitive impairment. In this overview, the neurotoxic effects of environmental factors and their relationship with neurodegenerative diseases are briefly introduced. Further, aiming at the damage to the nervous system caused by metals such as aluminum, manganese, and iron, this special column attempted to evaluate the damage degree by combining objective imaging and cognitive scales and to explore the mechanism of toxicity (including neurotransmitter secretion disorders and tau protein hyperphosphorylation) by in vitro experiments. These papers also introduced intervention studies using hydrogen-rich water to target the damage of ionizing radiation to the nervous system and discussed the intervention mechanism as modulating the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT)/Caspase-9 pathway, and Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway.

     

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