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Toxicity of long term exposure to low dose polystyrene microplastics and nanoplastics in human iPSC-derived cardiomyocytes
Summary
Researchers exposed human heart cells grown from stem cells to very low doses of polystyrene micro- and nanoplastics over an extended period and found that the particles reduced the cells' ability to contract and disrupted their electrical signaling. The smaller nanoplastics (50 nm) caused more severe damage than the larger microplastics (1 micrometer), including increased cell death and calcium handling problems. This study provides direct evidence that even low-level microplastic exposure could harm human heart function.
Microplastics and nanoplastics (MNPs) are widespread environmental pollutants with potential risks to human health including cardiovascular effects. However, the impact of MNPs on the heart, particularly in human-relevant cardiac models, remains poorly understood. In this study, we investigated the long term effects of polystyrene (PS) MNPs-1 μm (PS-1) and 0.05 μm (PS-0.05) in human iPSC-derived cardiomyocytes (hiPSC-CMs). PS MNPs exposure reduced myocyte viability in a time- and dose-dependent manner. At a low dose of 0.1 μg/L, both PS-0.05 and PS-1 suppressed myocyte contractility, reduced Ca transient amplitude, and altered contraction and Ca transient dynamics. In hypertrophic hiPSC-CMs, PS-0.05 exposure exacerbated hypertrophy, increasing cell size and proBNP expression, a marker of myocyte hypertrophy. The mechanism of PS MNPs-induced cardiotoxicity likely involved mitochondrial dysfunction, as indicated by decreased mitochondrial membrane potential, increased mitochondrial ROS, and elevated intracellular ROS levels. This is the first study to assess the long term impact of low dose MNPs in human cardiomyocytes, providing crucial insight into the potential cardiac toxicity of MNPs and their implications for human heart health.
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