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Toxic effects of polystyrene and polyethylene microplastics on the zebrafish cardiovascular system and their differential mechanisms
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Researchers compared the cardiovascular toxicity of polystyrene and polyethylene microplastics in zebrafish larvae, examining effects on heart development, oxidative stress, and cell death. Both types of microplastics caused cardiovascular damage, but they operated through different molecular mechanisms, with polystyrene primarily triggering oxidative stress while polyethylene more strongly induced cell death pathways. The findings indicate that the chemical composition of microplastics matters significantly when assessing their health effects.
This study investigated the toxic effects of polystyrene (PS) and polyethylene (PE) microplastics on the cardiovascular systems of zebrafish, as well as the differences in their mechanisms. Using a larval zebrafish (Danio rerio) model, we systematically evaluate the effects of the two microplastics on growth and development, oxidative stress, myocardial cell number and structure, histopathological changes, cell apoptosis, and gene expression via physiological parameter measurements, histopathological analysis, and molecular biological techniques. The experimental results showed that PS exerted a more significant inhibitory effect on body weight, whereas PE had a more marked inhibitory effect on body length. Both substances caused a dose-dependent decrease in heart rate, induced oxidative stress, aggravated myocardial damage and fibrosis and activated inflammatory responses. Additionally, PS and PE microplastics exhibit differences in their toxic mechanisms. PS enhances toxicity primarily through the adsorption capacity of its rigid benzene ring structures. While PE, due to its strong hydrophobicity, tends to accumulate more readily in myocardial tissue and exacerbate cell apoptosis via physical damage pathways. This study is the first to compare the differential mechanisms of cardiovascular toxicity between PS and PE microplastics in zebrafish, providing scientific evidence for environmental risk assessment and human health protection related to microplastics.
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