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通过人类发育神经毒理学的不良结果通路 (AOP) 网络,识别和多基基物质 (PFAS) 可能对神经发育的影响

Sayed Esmaeil Mousavi¹, Maryam Zarean², Jimmy Yu¹

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

The Science of the total environment

|December 19, 2025

概括

早期暴露于和多基基物质 (PFAS) 可能会损害神经发育. 这项研究确定甲状腺激素干扰和过载是导致PFAS暴露导致发育神经毒性 (DNT) 的关键机制.

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:

在早期暴露于基和多基物质 (PFAS) 和神经发育结果之间存在不一致的关联.
通过PFAS诱导发育神经毒性 (DNT) 的确切机制尚不清楚.
需要采用统一的网络方法来阐明DNT路径.

研究的目的:

为发展性神经毒性 (DNT) 开发第一个统一的不良结果途径 (AOP) 网络.
确定关键的机制性途径,将PFAS暴露与DNT联系起来.
为DNT的体外测试电池的开发提供信息.

主要方法:

从AOP-Wiki中检索了343个AOP,选择了与DNT相关的19个线性AOP.
构建了一个DNT-AOP网络并使用拓指标对其进行分析.
应用证据权重 (WoE) 评估与网络分析一起,以确定关键路径.

主要成果:

确定了两个关键途径:甲状腺激素的干扰和细胞内 (Ca2+) 的过载.
PFAS暴露与神经细胞中甲状腺素水平降低和细胞内Ca2+升高有机械联系.
这些干扰与突触生成,神经可塑性,神经元连接性和认知缺陷的损害有关.

结论:

甲状腺激素的干扰和Ca2+过载是介导PFAS诱导的DNT的关键机制.
这些发现凸显了在DNT测试中测量BDNF,细胞内Ca2+,甲状腺素和质炎症的测定方法的需要.
这种机制框架支持对与PFAS相关的发育神经毒性进行风险评估.

关键词:

在AOP网络网络中,AOP网络是AOP网络.的调节失调的调节失调认知缺陷认知缺陷发育神经毒性测试发育神经毒性测试神经发育障碍神经发育障碍甲状腺激素的破坏甲状腺激素的破坏

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