Oxidative stress-activated Nrf2 remitted polystyrene nanoplastic-induced mitochondrial damage and inflammatory response in HepG2 cells

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.