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Differences in toxicity induced by the various polymer types of nanoplastics on HepG2 cells

The problem of microplastics (MPs) contamination in food has gradually come to the fore. MPs can be transmitted through the food chain and accumulate within various organisms, ultimately posing a threat to human health. The concentration of nanoplastics (NPs) exposed to humans may be higher than tha...

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Published in:The Science of the total environment 2024-03, Vol.918, p.170664-170664, Article 170664
Main Authors: Ma, Lihua, Wu, Zijie, Lu, Zifan, Yan, Linhong, Dong, Xiaoling, Dai, Zhenqing, Sun, Ruikun, Hong, Pengzhi, Zhou, Chunxia, Li, Chengyong
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Language:English
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Summary:The problem of microplastics (MPs) contamination in food has gradually come to the fore. MPs can be transmitted through the food chain and accumulate within various organisms, ultimately posing a threat to human health. The concentration of nanoplastics (NPs) exposed to humans may be higher than that of MPs. For the first time, we studied the differences in toxicity, and potential toxic effects of different polymer types of NPs, namely, polyethylene terephthalate (PET), polyvinyl chloride (PVC), and polystyrene (PS) on HepG2 cells. In this study, PET-NPs, PVC-NPs, and PS-NPs, which had similar particle size, surface charge, and shape, were prepared using nanoprecipitation and emulsion polymerization. The results of the CCK-8 assay showed that the PET-NPs and PVC-NPs induced a decrease in cell viability in a concentration-dependent manner, and their lowest concentrations causing significant cytotoxicity were 100 and 150 μg/mL, respectively. Moreover, the major cytotoxic effects of PET-NPs and PVC-NPs at high concentrations may be to induce an increase in intracellular ROS, which in turn induces cellular damage and other toxic effects. Notably, our study suggested that PET-NPs and PVC-NPs may induce apoptosis in HepG2 cells through the mitochondrial apoptotic pathway. However, no relevant cytotoxicity, oxidative damage, and apoptotic toxic effects were detected in HepG2 cells with exposure to PS-NPs. Furthermore, the analysis of transcriptomics data suggested that PET-NPs and PVC-NPs could significantly inhibit the expression of DNA repair-related genes in the p53 signaling pathway. Compared to PS-NPs, the expression levels of lipid metabolism-related genes were down-regulated to a greater extent by PET-NPs and PVC-NPs. In conclusion, PET-NPs and PVC-NPs were able to induce higher cytotoxic effects than PS-NPs, in which the density and chemical structure of NPs of different polymer types may be the key factors causing the differences in toxicity. [Display omitted] •PET-NPs, PVC-NPs, and PS-NPs with similar size and surface charge were prepared for toxicological evaluation.•PET-NPs and PVC-NPs were more toxic to the HepG2 cells than PS-NPs.•PET-NPs and PVC-NPs induced oxidative stress and apoptosis in HepG2 cells in a dose-dependent manner.•ROS might be the key factor contributing to the higher cytotoxicity induced by PET-NPs and PVC-NPs.•PET-NPs, PVC-NPs and, PS-NPs affected the gene expression profile in the HepG2 cells at different degrees.
ISSN:0048-9697
1879-1026
DOI:10.1016/j.scitotenv.2024.170664