Abstract
Polystyrene (PS) nanoplastic exposure has been shown to affect the viability of neuronal cells isolated from mouse embryonic brains. However, the viability of mouse embryonic fibroblasts (MEFs) was not affected although PS nanoplastics accumulated in the cytoplasm. It is currently unknown whether MEFs do not respond to PS nanoplastics or their cellular functions are altered without compromising viability. Here, we found that PS nanoplastics entered the cells via endo-cytosis and were then released into the cytoplasm, probably by endosomal escape, or otherwise remained in the endosome. Oxidative and inflammatory stress caused by intracellular PS nano-plastics induced the antioxidant response pathway and activated the autophagic pathway. How-ever, colocalization of the autophagic marker LC3B and PS nanoplastics suggested that PS nano-plastics in the cytoplasm might interfere with normal autophagic function. Furthermore, au-tophagic flux could be impaired, probably due to accumulation of PS nanoplastic-containing ly-sosomes or autolysosomes. Intriguingly, the level of accumulated PS nanoplastics decreased during prolonged culture when MEFs were no longer exposed to PS nanoplastics. These results indi-cate that accumulated PS nanoplastics are removed or exported out of the cells. Therefore, PS na-noplastics in the cytoplasm affect cellular functions, but it is temporal and MEFs can overcome the stress caused by PS nanoplastic exposure.
Original language | English |
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Article number | 2094 |
Pages (from-to) | 1-11 |
Number of pages | 11 |
Journal | International Journal of Molecular Sciences |
Volume | 22 |
Issue number | 4 |
DOIs | |
State | Published - 2 Feb 2021 |
Keywords
- Autophagy
- Endocytosis
- MEFs
- Nanoplastic
- Oxidative stress
- Polystyrene