Abstract
Plastics play a crucial role in nearly each aspect of societal production and everyday life, therefore making them one of the most widespread pollutants on a global scale. Because synthetic plastics are not entirely biodegradable, they often remain in the environment and fragment into micro- and nanoplastic particles. The detrimental impacts of nanoplastics on the environment and human health have received substantial worldwide interest in recent years. However, the effects of nanoplastics on human health have not yet been fully explored. Our study aimed to investigate the cytotoxic effects of polystyrene nanoplastics on two distinct mammalian cell lines: normal rat kidney cells (NRK52E) and human umbilical vein endothelial cells (HUVECs). Results showed that polystyrene nanoplastics generate cytotoxicity in both NRK52E and HUVECs in a concentration- and time-dependent manner. Additionally, polystyrene nanoplastics induced pro-oxidant levels (e.g., reactive oxygen species and hydrogen peroxide) and reduced antioxidants (glutathione content and glutathione peroxidase enzyme activity) in both types of cells. We also found that polystyrene nanoplastics cause apoptosis in both NRK52E and HUVECs, as shown by the activation of the caspase-3 enzyme and the loss of mitochondrial membrane potential. Interestingly, it was noticed that the vulnerability of HUVECs cells against polystyrene nanoplastics was a little higher than that of NRK52E cells. Also, the cell toxicity caused by polystyrene nanoplastics in NRK52E and HUVECs was effectively alleviated by co-exposure to a reactive oxygen species inhibitor, N-acetyl-cysteine. This suggests that oxidative stress could be one of the possible pathways by which polystyrene nanoplastics cause cell toxicity. The present work warrants future study to explore the toxicity mechanisms of polystyrene nanoplastics in appropriate in vivo models.
Published Version
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