Polystyrene nanoplastics induced toxicity in human endothelial cells via atherogenic and autophagy pathways

Polystyrene nanoplastics (PS NPs) pollution poses an emerging threat to the ecosystem and human health owing to their physicochemical properties. Excessive exposure to PS NPs can disrupt the cardiovascular system, especially the function of endothelial cells (ECs). Given the potential pathological significance of particles, the present study aimed to investigate the cytotoxic effects of PS NPs on ECs in in vitro and ex ovo models, as well as their underlying mechanisms.

PS NPs were characterized using DLS, SEM, and FTIR. Human umbilical vein ECs (HUVECs) were first treated with 5 and 100 µg/ml PS NPs for all in vitro assays. Cellular uptake of PS NPs was monitored by flow cytometry, and the interaction of PS NP-treated HUVECs with peripheral blood mononuclear cells was evaluated using surface plasmon resonance (SPR). Protein and cDNA adsorption onto PS NPs were analyzed by SDS-PAGE and agarose gel electrophoresis, respectively. A PCR array was also utilized for analyzing atherogenic and autophagy pathways. For ex ovo toxicity assessment, chicken embryos were exposed to 40 µg/ml PS NPs for 7 days. Then, the heart samples of embryos were investigated for PS NPs internalization and histopathological changes by DAPI and hematoxylin and eosin staining, respectively.

PS NPs were taken up by HUVECs, especially at a 5 µg/ml dose. The protein corona formed on the surface of PS NPs, without being affected by cDNA. SPR analysis revealed that PS NPs altered the interaction of endothelial and immune cells. Exposure to PS NPs could induce changes in atherogenic and autophagy pathways in ECs. Histopathological analyses of chicken embryos indicated cardiac damage and the accumulation of PS NPs in cardiac tissue after 7 days of exposure.

Taken together, these findings indicated that PS NPs may dose-dependently induce endothelial dysfunction in ECs and histopathological damage in the cardiac tissue of chicken embryos. These toxic effects were likely mediated through affecting autophagy and atherosclerotic pathways, and the interaction of endothelial-immune cells. Therefore, the results emphasize the high potential for toxicity and cardiovascular risks associated with PS NPs.