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急性Cu暴露通过DAF-16/FoxO和SKN-1/Nrf2通路诱导神经毒性

Ying Zhang¹, Peixin Lu¹, Pai Peng¹

¹Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China.

Journal of environmental sciences (China)

|July 2, 2025

概括

急性铜 (Cu) 暴露会损害C. elegans的神经系统,损害行为和神经元功能. 这项研究揭示了Cu诱导的神经毒性涉及氧化应激和特定的转录因子,SKN-1和DAF-16.

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.
分子生物学分子生物学

背景情况:

由于其毒性和持久性,铜 (Cu) 污染是一个全球性问题.
代谢的失衡与神经退行性疾病有关.
以前的研究表明,Cu通过氧化应激和细胞功能障碍导致神经毒性,但机制尚不清楚.

研究的目的:

为了研究急性铜暴露在Caenorhabditis elegans中的神经毒性影响.
阐明Cu诱导的神经毒性的潜在分子机制.

主要方法:

暴露于不同度的Cu (0.01-10毫克/升) 的C. elegans.
评估运动和感官行为.
分析神经元完整性 (多巴胺,谷氨酸,GABA,胆固醇) 和神经递质表达.
研究氧化应激标志物和转录因子活性 (SKN-1,DAF-16).
利用C. elegans突变体 (skn-1, daf-16) 来研究基因调节.

主要成果:

对Cu的暴露抑制了C. elegans的运动和感官行为.
这损害了关键神经元,并降低了神经递质表达.
暴露促进了氧化应激,并改变了SKN-1和DAF-16.6的核定位.
skn-1和daf-16突变体对Cu诱导的行为缺陷的敏感性增加.
通过SKN-1和DAF-16.4进行下游调节的基因 (sod-3,ctl-1,gcs-1,gst-4)

结论:

急性铜暴露会诱导C. elegans的神经毒性,影响行为和神经元健康.
该研究确定氧化应激和转录因子SKN-1和DAF-16是Cu神经毒性的关键因素.
在应对神经毒性时,Cu通过SKN-1和DAF-16调节特定的抗氧化和排毒基因.

关键词:

凯诺哈比迪斯 (Caenorhabditis elegans) 是一个可怕的生物.暴露于Cu中的Cu暴露.在DAF-16/FoxOO中使用.神经毒性神经毒性在SKN-1/ Nrf2中使用.

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