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Toxic effects of nanoplastics on a model of dog aortic cells
Summary
Researchers exposed dog aortic endothelial cells to nanoplastic fragments and observed that the particles entered cells and localized in the cytoplasm. The nanoplastics disrupted cell proliferation and metabolic activity while inducing oxidative stress through increased reactive oxygen species production. The study suggests that nanoplastics can directly damage vascular cells, raising questions about potential cardiovascular effects of nanoplastic exposure.
Nanoplastic fragments (NP) are a growing concern and using dog aortic endothelial cells (CnAEOC) and fluorescence microscopy, we observed an interaction between NP and cells, demonstrating a localization at the cytoplasmic level. Furthermore, the data collected show a disruption of both cell proliferation and metabolic activity. The results also show the induction of oxidative stress. In detail, NP caused an increase in the levels of ROS production and an inhibition of enzymatic defence systems. On the contrary, there was no alteration of the non-enzymatic defence mechanism. The analysis conducted to evaluate a possible induction of autophagy, a survival mechanism implemented by cells, following exposure to NP reported the absence of autophagy involvement in the model analysed. Finally, investigations were conducted regarding the involvement of NP in gene expression processes. Both RNA-seq and RT-PCR did not highlight differentially expressed genes in treated cells.
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