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[Polystyrene nanoplastics disrupt macrophage cholesterol metabolism by adsorbing apolipoprotein E].
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Researchers used proteomic analysis combined with molecular docking and dynamics simulations to show that polystyrene nanoplastics selectively adsorb apolipoprotein E (APOE) in macrophages by occupying key binding residues, blocking APOE–cholesterol interaction and causing intracellular lipid accumulation—identifying a molecular mechanism that may explain how nanoplastic exposure promotes atherosclerosis risk.
This study aimed to investigate the potential health hazards and molecular mechanisms of nanoplastic (NP) pollutants. Polystyrene nanoplastics (PS-NPs), which are prevalent in the environment and can enter the human body, have been closely associated with the risk of cardiovascular diseases, yet their impact on cholesterol metabolism remains unclear. In this study, proteomic analysis revealed that PS-NPs specifically adsorbed 1 676 proteins following their interaction with macrophages. Bioinformatic analysis indicated that these adsorbed proteins were significantly enriched in the cholesterol metabolism pathway, with apolipoprotein E (APOE) being the most prominently adsorbed. Further molecular docking and molecular dynamics simulations demonstrated that polystyrene molecules could inhibit the interaction between APOE and cholesterol by competitively binding to key amino acid residues (e.g., LEU-202 and TRP-228) of APOE. Cell experiments confirmed that exposure to 100 μg/mL PS-NPs for 24 h significantly induced lipid accumulation in macrophages. This study reveals, from a molecular interaction perspective, a novel mechanism by which PS-NPs disrupt lipid metabolism by interfering with APOE function. It provides key evidence for elucidating the toxicological mechanism through which PS-NPs promote atherosclerosis and holds significant scientific importance for assessing their health risks.
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Polystyrene nanoplastics dysregulate lipid metabolism in murine macrophages in vitro
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Researchers investigated the effects of polystyrene nanoplastics on immune cell metabolism and found that macrophages exposed to nanoplastics transformed into lipid-laden foam cells. The study suggests that nanoplastic exposure dysregulates lipid metabolism in immune cells, with implications for understanding how these particles may interact with the immune system at the cellular level.
The effects of adsorbed benzo(a)pyrene on dynamic behavior of polystyrene nanoplastics through phospholipid membrane: A molecular simulation study
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Researchers used molecular simulations to show that benzo(a)pyrene adsorbed onto polystyrene nanoplastics alters how the particles interact with and penetrate phospholipid membranes, suggesting that pollutant-coated nanoplastics may pose different biological risks than pristine ones.
[The effect and mechanism of exposure to polystyrene nanoplastics on lipid metabolism in mice liver].
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Researchers exposed mice to 20 nm polystyrene nanoplastics and investigated the effects on hepatic lipid metabolism using multi-omics approaches. Nanoplastic exposure disrupted lipid metabolic pathways in the liver, causing significant changes in lipid accumulation and related gene expression, suggesting a mechanism by which nanoplastic ingestion may contribute to metabolic disorders.
Modelling bionano interactions and potential health risks for environmental nanoplastics: the case of functionalized polystyrene
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Researchers used computer simulations to model how proteins adsorb onto polystyrene nanoplastic surfaces, investigating bionano interactions relevant to potential health risks. The study focused on functionalized polystyrene as a model for environmental nanoplastics. The findings contribute to understanding how nanoplastics interact with biological molecules, which is important for evaluating their toxicological potential.
Polystyrene Nanoplastic Contaminants Denature Human Apolipoprotein A-1
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Researchers used advanced spectroscopy techniques to study what happens when a key human blood protein, apolipoprotein A-1, comes into contact with polystyrene nanoplastics. They found that the protein changes its structure and forms abnormal fibrillar clumps at the nanoplastic surface, causing the plastic particles to cluster together. Since apolipoprotein A-1 is important for cholesterol transport, these structural changes at the nanoplastic interface may pose risks to cardiovascular health.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.