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通过一个不良结果通路网络探索per-和多基基物质的神经退行潜力

Sayed Esmaeil Mousavi¹, Jimmy Yu¹, Hyeong-Moo Shin²

¹School of Engineering and Built Environment, Griffith University, Nathan Campus, QLD 4111, Australia.

The Science of the total environment

|March 1, 2025

概括

和多醇基物质 (PFAS) 可能通过破坏信号传递和引起神经元亡,从而导致神经元退行. 这项研究开发了一个不良结果途径 (AOP) 网络,以探索PFAS的神经毒性机制,特别是对于阿尔茨海默氏症和帕金森病.

科学领域:

环境毒理学环境毒理学
神经科学是一个神经科学.
计算毒理学计算毒理学

背景情况:

新出现的证据表明,per-和多醇基物质 (PFAS) 具有神经毒性,但它们在神经退行中的作用尚不清楚.
对于神经退行现有的不良结果途径 (AOP) 并没有被整合到一个统一的网络中.
了解PFAS的神经毒性对于公共卫生和监管评估至关重要.

研究的目的:

开发第一个与神经退行相关的AOP网络.
探索长链遗留PFAS对神经退行症 (包括阿尔茨海默氏症和帕金森病) 的贡献.
阐明PFAS暴露和神经退行性途径之间的机制联系.

主要方法:

从AOP-Wiki中选了74个AOP,选择了13个与神经退行相关的AOP.
使用拓参数构建和分析了与神经退行相关的AOP网络.
综合证据将PFAS暴露与AOP网络中的关键事件 (KE) 联系起来.

主要成果:

确定了细胞内的增加作为网络枢纽,其次是神经退行,神经细胞亡,氧化应激,N-甲基-d-酸盐受体 (NMDA-R) 过度活化和线粒体功能障碍.
该AOP网络建议PFAS通过NMDA-R过度激活对神经递质系统产生不利影响,导致兴奋毒性.
暴露于PFAS可能会导致体平衡,线粒体功能障碍,炎症-氧化级联,神经炎症和神经元细胞死亡.

结论:

本研究提供了PFAS神经退行潜力的机制框架,突出了关键途径.
这些发现表明,PFAS可能会导致神经退行性疾病,如阿尔茨海默氏症和帕金森症.
需要进一步的实验验证,以在相关模型中确认这些机制联系.

关键词:

负面结果的途径.二氧化碳平衡作用 (dishomeostasis) 的原因线粒体功能障碍线粒体功能障碍神经退行发生神经退行.神经元的亡是神经元的亡.在PFAS中,我们可以使用PFAS.

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