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Aged microplastics disrupted copper homeostasis to induce vascular toxicity: in vivo and human vascular organoids-based in vitro study
Summary
Researchers evaluated the vascular toxicity of aged polypropylene microplastics using both human vascular organoids and in vivo models, finding that aged microplastics disrupted copper homeostasis in blood vessel cells. This copper imbalance led to oxidative stress and damage to the vascular endothelium. The study suggests that the aging process microplastics undergo in the environment may make them more harmful to the cardiovascular system than fresh particles.
Microplastics (MP), as pervasive environmental pollutants, inevitably undergo ageing processes, resulting in the formation of aged MP (aMP). Humans are chronically exposed to aMP, posing potential health risks. As the primary circulatory conduits, blood vessels play a critical role in systemic MP distribution following exposure through multiple routes. However, the vascular toxicity of MP remains poorly understood. The vascular toxicity of aged polypropylene MP (aPP) was evaluated using human embryonic stem cell-derived vascular organoids (VOs) and Balb/c mice, with doses reflecting human internal exposure levels. It was observed that aPP induced cytotoxicity, dysregulated lysyl oxidase (LOX) and Elastin expression, and caused vascular structural abnormalities. Additionally, aPP disrupted copper (Cu) homeostasis, manifested through significantly upregulated SLC31A1, ATOX1, COX17, FDX1, and DLAT expression, along with downregulated ATP7B and LOX levels. Reductive stress was also induced, featuring elevated SOD, NADH, GSH-Px, and reduced MDA contents. Collectively, these results indicate that aPP disrupted Cu homeostasis and induced reductive stress both in vitro and in vivo, suggesting a potential threat to vascular health.
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