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Polystyrene nanoplastics induce apoptosis of human kidney proximal tubular epithelial cells via oxidative stress and MAPK signaling pathways

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Polystyrene nanoplastics (PS-NPs) have recently been found to be present in human blood and kidney. However, the renal toxicity of PS-NPs and the underlying mechanisms have not been fully elucidated. Here, we found that exposure of PS-NPs induced apoptosis of human renal proximal tubular epithelial cells (HK-2) in a size- and dose-dependent manner as revealed by AnnexinV-FITC assay. In addition, PS-NPs promoted ROS production and caused structure changes of mitochondrial and endoplasmic reticulum. Mechanistically, transcriptional sequencing indicated the involvement of MAPK pathway in apoptosis, which was further confirmed by the upregulation of p-p38, p-ERK, CHOP, BAX, cytochrome C, and caspase 3 expression. This study clarified the molecular mechanism underlying PS-NP-induced apoptosis in HK-2 cells and contributed to our risk estimation of PS-NPs in human kidney.

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The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

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Funding

This work was supported by the National Natural Science Foundation of China (82170523, 81870261), Sichuan Youth Science and Technology Innovation Research Team (2020JDTD0024), Sichuan Science and Technology Program (2022YFS0610), and Collaborative Innovation Center for the Prevention and Treatment of Cardiovascular Diseases in Sichuan Province (xtcx2016-14, xtcx 2019-06).

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All authors contributed to the study conception and design. Material preparation, data collection, and analysis were performed by Zhu Zhu. Ruixue Liao, and Yang Shi. The first draft of the manuscript was written by Zhu Zhu, Jingyan Li, Guang Li. All authors read and approved the final manuscript.

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Correspondence to Guang Li.

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Zhu, Z., Liao, R., Shi, Y. et al. Polystyrene nanoplastics induce apoptosis of human kidney proximal tubular epithelial cells via oxidative stress and MAPK signaling pathways. Environ Sci Pollut Res 30, 110579–110589 (2023). https://doi.org/10.1007/s11356-023-30155-x

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