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聚乙烯纳米塑料诱导的肺亡和铁亡通过ROS依赖的内质网膜应激作用

Qiumei Wu¹, Chao Liu¹, Dan Liu¹

¹Brain Science and Advanced Technology Institute, Hubei Province Key Laboratory of Occupational Hazard Identification and Control, School of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China.

The Science of the total environment

|December 12, 2023

概括

聚乙烯纳米塑料 (PS-NP) 通过激活内质网膜压力,通过亡和铁亡引起肺损伤. N-乙半氨酸 (NAC) 通过抑制这种ROS依赖途径来保护PS-NP的毒性.

科学领域:

环境毒理学环境毒理学
纳米材料的安全性
毒性的细胞机制.

背景情况:

吸入纳米塑料 (MNP) 的暴露可能导致肺毒性.
呼吸系统中MNP的确切毒理机制尚未完全理解.

研究的目的:

在BEAS-2B细胞和小鼠中研究聚乙烯纳米塑料 (PS-NP) 的毒理机制.
阐明亡,铁亡和内细胞网膜 (ER) 应激在PS-NP诱导的肺损伤中的作用.
评估N-乙半氨酸 (NAC) 对PS-NP毒性的保护作用.

主要方法:

将BEAS-2B细胞和小鼠暴露在不同度的PS-NP中.
评估氧化应激,亡 (流细胞计),铁亡标志物 (GPX4,FTH1,铁含量,MDA),线粒体功能和ER应激蛋白 (IRE1α,PERK,XBP1S,CHOP).
用ROS抑制剂NAC来评估其保护作用.

主要成果:

在细胞和小鼠中,PS-NPs诱导了氧化应激,亡,铁亡,线粒体功能障碍,并增加了MDA水平.
PS-NP激活了两个主要的ER应激通路 (IRE1α和PERK).
通过抑制ROS依赖的ER压力,NAC治疗减轻了PS-NP诱导的肺损伤.

结论:

通过ER应激的介导,PS-NPs通过亡和铁亡诱导肺损伤和细胞死亡.
通过抑制ROS依赖的ER压力,NAC证明了对PS-NP毒性的保护作用.
这项研究增强了对纳米塑料肺毒性机制和潜在治疗干预措施的理解.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.细胞内膜网膜 (ER) 应激压力铁化是铁化的一种.微塑料是一种微塑料.纳米塑料是一种纳米塑料.

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