氧化应激
活性氧
微塑料
炎症
线粒体
化学
线粒体ROS
细胞生物学
KEAP1型
生物化学
免疫学
生物
转录因子
环境化学
基因
作者
Menghao Guo,Yunjing Li,Shuyan Niu,Rui Zhang,Xipeng Shen,Yuanyuan Ma,Liqing Wu,Tianshu Wu,Ting Zhang,Tao Meng,Xue Yang
标识
DOI:10.1016/j.etap.2024.104385
摘要
Generated from plastics, microplastics (MPs) and nanoplastics (NPs) are difficult to completely degrade in the natural environment, which can accumulate in almost all lives. Liver is one of the main target organs. In this study, HepG2 and L02 cells were exposed to 0–50 μg/mL polystyrene (PS)-NPs to investigate the mechanism of mitochondrial damage and inflammation. The results showed mitochondria damage and inflammatory caused by NPs, and it can be inhibited by N-acetyl-L-cysteine (NAC). In addition, reactive oxygen species (ROS) activated nuclear factor erythroid-derived factor 2-related factor (Nrf2) pathway. Nrf2 siRNA exacerbated the injury, suggesting Nrf2 plays a protective role. Moreover, p62 siRNA increased ROS and mitochondrial damage by inhibiting Nrf2, but didn't affect the inflammation. In conclusion, Nrf2 was activated by ROS and played a protective role in PS-NPs-mediated hepatotoxicity. This study supplemented the data of liver injury caused by PS-NPs, providing a basis for the safe disposal of plastics.
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