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Toxic effects of nanoplastics with different sizes and surface charges on epithelial-to-mesenchymal transition in A549 cells and the potential toxicological mechanism

Journal of Hazardous Materials 2022 190 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.

Gulinare Halimu, Gulinare Halimu, Gulinare Halimu, Zhichun Zhang, Gulinare Halimu, Mingkai Xu, Zhichun Zhang, Yumeng Dai, Qianru Zhang, Gulinare Halimu, Yumeng Dai, Mingkai Xu, Qianru Zhang, Mingkai Xu, Gulinare Halimu, Qianru Zhang, Qianru Zhang, Zhichun Zhang, Qianru Zhang, Qianru Zhang, Qianru Zhang, Qianru Zhang, Li Liu, Qianru Zhang, Qianru Zhang, Mingkai Xu, Zhichun Zhang, Zhichun Zhang, Zhichun Zhang, Wu Gu, Gulinare Halimu, Wu Gu, Gulinare Halimu, Yumeng Dai, Xiujuan Wang, Wu Gu, Wu Gu, Wu Gu, Wu Gu, Wu Gu, Wu Gu, Bowen Zhang, Yumeng Dai, Xiujuan Wang, Yumeng Dai, Huiwen Zhang, Xiujuan Wang, Mingkai Xu, Huiwen Zhang, Qianru Zhang, Chenggang Zhang Yumeng Dai, Mingkai Xu, Yumeng Dai, Huiwen Zhang, Mingkai Xu, Chenggang Zhang

Summary

Researchers exposed human lung cells to polystyrene nanoplastics of different sizes and surface charges and found they triggered a process called epithelial-to-mesenchymal transition, which is associated with the early stages of lung fibrosis. Smaller particles and those with positive surface charges caused the strongest effects, activating oxidative stress and inflammatory pathways. The study suggests that inhaled nanoplastics could contribute to respiratory health risks by promoting tissue scarring in the lungs.

Polymers

Body Systems

Immune Respiratory

As a newly emerging hazardous material, airborne nanoplastics are easily inhaled and accumulated in human and animal alveoli. We previously found that polystyrene nanoplastics (PS-NPs) induced apoptosis and inflammation of human alveolar epithelial A549 cells, implying they increase the risk of pulmonary fibrosis. In this study, we investigated whether PS-NPs induce epithelial-to-mesenchymal transition (EMT), the prelude to lung fibrosis, in A549 cells. A549 cells treated with PS-NPs of different sizes and surface charges exhibited increased migration and EMT markers accompanied with up-regulation of reactive oxygen species (ROS) and NADPH oxidase 4 (NOX4), an ROS generator located in the mitochondria and endoplasmic reticulum (ER). Moreover, PS-NPs caused mitochondrial dysfunction as demonstrated by membrane potential changes and impaired cellular energy metabolism. PS-NPs also activated ER stress as indicated by the up-regulated ER stress markers. As expected, smaller PS-NPs with a positive surface charge had stronger effects. Furthermore, the effects of PS-NPs on A549 cells were reversed by NOX4 gene knock-down, which verified the involvement of NOX4. Our results suggest that PS-NPs induce EMT in A549 cells through multiple mechanisms, and NOX4 is a key mediator in this process. Our findings contribute to understanding the toxicological mechanisms of nanoplastics on the respiratory system.

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