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Exposure to polystyrene microplastics with different functional groups: Implications for blood pressure and heart

Environmental Pollution 2025 13 citations

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In a rat study, exposure to polystyrene microplastics raised blood pressure by 22-40% and caused heart muscle enlargement and oxidative damage, with chemically modified microplastics causing even worse effects. The research identified a molecular pathway involving reduced blood vessel-relaxing signals that may explain how microplastic exposure contributes to cardiovascular disease.

Polymers
Body Systems
Models

The association between microplastics (MPs) exposure and cardiovascular disease is largely unknown. It is still unclear what effects MPs exposure have on blood pressure and how it affects the heart. As MPs age, their surfaces undergo modifications that may alter how the MPs interact with cells, which may affect the extent of their toxic effects. Here, we used three different surface functional-group polystyrene microplastics (PS-MPs), and exposed 5-week-old SD rats to them over 42 days. Compared with the control group, the mean blood pressure of the MPs exposed rats increased by 22-40%. Exposure to PS-MPs caused oxidative damage to the heart, and induced cardiomyocyte hypertrophy. More interestingly, MPs modified by functional groups induced enhanced adverse effects than unmodified PS-MPs, with amino-modified PS-MPs exhibiting more significant blood pressure elevation and myocardial hypertrophy. Proteomic analysis of cardiac differential proteins focused on factor XII activation, negative regulation of proteolysis, collectively pointed to the downregulation of kininogen. We demonstrated that MPs exposure induced ERK activation, the down-regulation of bradykinin, and inhibition of the downstream nitric oxide signaling pathway. This study demonstrates the different effects of MPs with different functional groups on blood pressure elevation and myocardial hypertrophy, and sheds light on the mechanisms responsible for microplastic-induced cardiovascular toxicity.

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