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The effect of polystyrene nanoplastics on arsenic-induced apoptosis in HepG2 cells
Summary
Researchers studied the combined effects of polystyrene nanoplastics and arsenic on human liver cells in the laboratory. They found that nanoplastics, particularly those around 50 nanometers in size, significantly enhanced arsenic-induced cell death by disrupting mitochondrial function. The study identifies key genes involved in this interaction, suggesting that microplastic exposure may worsen the toxic effects of heavy metals on liver cells.
Microplastics are detrimental to the environment. However, the combined effects of microplastics and arsenic (As) remain unclear. In this study, we investigated the combined effects of polystyrene (PS) microplastics and As on HepG2 cells. The results showed that PS microplastics 20, 50, 200, and 500 nm in size were taken up by HepG2 cells, causing a decrease in cellular mitochondrial membrane potential. The results of lactate dehydrogenase release and flow cytometry showed that PS microplastics, especially those of 50 nm, enhanced As-induced apoptosis. In addition, transcriptome analysis revealed that TP53, AKT1, CASP3, ACTB, BCL2L1, CASP8, XIAP, MCL1, NFKBIA, and CASP7 were the top 10 hub genes for PS that enhanced the role of As in HepG2 cell apoptosis. Our results suggest that nano-PS enhances As-induced apoptosis. Furthermore, this study is important for a better understanding of the role of microplastics in As-induced hepatotoxicity.