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20 resultsShowing papers similar to Polystyrene nanoplastics induced lung injury in mice: Insights into lung metabolic disorders
ClearIntegrated transcriptomics and metabolomics reveal the mechanism of polystyrene nanoplastics toxicity to mice
Researchers used gene expression and metabolic profiling to understand how polystyrene nanoplastics harm mice at the molecular level, finding disrupted energy metabolism, fat processing, and amino acid pathways in the liver. These molecular changes suggest that nanoplastic exposure could contribute to metabolic disorders, with effects becoming more severe at higher doses.
Unveiling the Pulmonary Toxicity of Polystyrene Nanoplastics: A Hierarchical Oxidative Stress Mechanism Driving Acute–Subacute Lung Injury
Researchers investigated the pulmonary toxicity of polystyrene nanoplastics smaller than 100 nm in lung epithelial cells and macrophages, finding that exposure triggered a hierarchical oxidative stress mechanism that drove acute to subacute lung injury through lipid peroxidation and inflammation.
Polystyrene nanoplastics reprogramed pulmonary metabolisms mediated by immune regulation of myeloid hypoxia-inducible factor 1α
Researchers exposed mice to polystyrene nanoplastics through their lungs for six weeks and found the particles triggered lung inflammation, scarring, and a metabolic switch to glycolysis — the same energy-burning pattern seen in activated immune cells during injury. A key protein called HIF-1α in immune cells was identified as the driver of these metabolic changes, offering a potential target for understanding nanoplastic lung toxicity.
Inhalation exposure to polystyrene nanoplastics induces chronic obstructive pulmonary disease-like lung injury in mice through multi-dimensional assessment
Mice that inhaled polystyrene nanoplastics developed lung damage resembling chronic obstructive pulmonary disease (COPD), including reduced breathing function, inflammation, and oxidative stress that worsened with longer exposure. The study found that nanoplastics caused this damage by disrupting mitochondria and triggering a type of cell death called ferroptosis, suggesting that breathing in airborne nanoplastics could increase the risk of serious lung disease.
Pulmonary toxicity of polymethyl methacrylate nanoplastics via intratracheal intubation in mice
Researchers exposed mice to polymethyl methacrylate nanoplastics through inhalation over 28 days to study their lung effects. The exposed mice experienced weight loss, nanoplastic accumulation in the lungs, increased inflammatory cell counts, and elevated inflammatory cytokines. The findings demonstrate that inhaling these common nanoplastics can induce lung inflammation, tissue damage, and changes in protein and RNA expression.
Inhaled polystyrene nanoparticles may cause fibrotic lesions via immune dysregulation and energy metabolism disturbance
Mice received polystyrene nanoparticles via pharyngeal instillation for 90 days and were assessed for local lung and systemic toxicity. The nanoparticles accumulated in lungs and hearts, caused immune dysregulation, disrupted energy metabolism, and induced fibrotic lesions at higher doses, suggesting that chronic inhalation of nanoplastics may contribute to pulmonary fibrosis.
Microplastics and nanoplastics, emerging pollutants, increased the risk of pulmonary fibrosis in vivo and in vitro: A comparative evaluation of their potential toxicity effects with different polymers and size
Researchers compared the lung toxicity of microplastics and nanoplastics made from polystyrene, polyethylene, and polypropylene in mice and human lung cells. They found that all particle types induced signs of pulmonary fibrosis, inflammation, and tissue remodeling, with polystyrene nanoplastics causing the most severe effects. The study suggests that smaller nanoplastic particles and certain polymer types may pose greater risks to lung health.
Repeated inhalation exposure to polystyrene nanoplastics induced sustained pulmonary injury and fibrosis in mice.
Scientists exposed mice to tiny plastic particles found in air pollution and discovered these particles caused serious lung damage and scarring that didn't heal even weeks after exposure stopped. The smallest plastic particles were the most harmful, spreading from the lungs to other organs like the heart and liver. This research suggests that breathing in nanoplastics from everyday sources like car tire wear and plastic waste could pose long-term risks to human lung health.
Polystyrene microplastic particles: In vitro pulmonary toxicity assessment
Researchers tested the effects of polystyrene microplastics on human lung cells in the laboratory and found that the particles triggered inflammation and oxidative stress. The microplastics also weakened the protective barrier function of lung tissue by depleting key structural proteins. The study suggests that inhaling microplastics may increase the risk of respiratory problems by damaging the lung's natural defenses.
Dynamic non-coding RNA biomarker reveals lung injury and repair induced by polystyrene nanoplastics
Researchers found that mice and lung organoids (lab-grown mini-organs) repeatedly exposed to polystyrene nanoplastics suffered lung tissue damage, impaired repair processes, and changes in non-coding RNA molecules that could serve as early warning biomarkers for nanoplastic-induced lung injury.
Internalization and toxicity: A preliminary study of effects of nanoplastic particles on human lung epithelial cell
Researchers studied the effects of polystyrene nanoplastic particles on human lung cells and found that the particles were internalized by the cells and caused dose-dependent toxicity. The nanoplastics triggered oxidative stress, inflammation, and disrupted normal cell function. The findings suggest that inhaling airborne nanoplastics may pose risks to respiratory health.
Integrative lipidomic and transcriptomic analysis unraveled polystyrene nanoplastics-induced liver injury via oral and inhalation exposure: All roads lead to Rome?
Researchers exposed mice to polystyrene nanoplastics through both oral ingestion and inhalation, and found that both routes caused liver damage but through different molecular pathways. Oral exposure mainly caused visible tissue damage, while inhaled nanoplastics triggered more severe inflammation and impaired the liver's ability to produce essential proteins. The study reveals that breathing in nanoplastics may be just as harmful to the liver as swallowing them, with different but equally concerning effects.
Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice
Researchers administered polystyrene microplastics directly into the lungs of mice and found that the particles induced pulmonary fibrosis by triggering oxidative stress and activating the Wnt signaling pathway. The microplastics caused damage to the lung lining cells and promoted the buildup of scar tissue in lung tissue. The study provides evidence that inhaled microplastics may contribute to serious respiratory conditions by driving fibrotic changes in the lungs.
Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice
This mouse study found that inhaling polystyrene microplastics caused serious lung damage, including inflammation, cell death, and scar tissue buildup. Smaller microplastics (1-5 micrometers) caused more harm than larger ones, and the damage worsened with longer exposure. The study identified a specific immune pathway (TLR2/NF-kB) through which inhaled microplastics trigger lung injury, raising concerns about the respiratory effects of airborne microplastics on humans.
Metabolomics reveals that PS-NPs promote lung injury by regulating prostaglandin B1 through the cGAS-STING pathway
Researchers found that polystyrene nanoplastics activate the cGAS-STING innate immune pathway in human lung cells and macrophages at near-environmental concentrations, causing mitochondrial dysfunction and metabolic disruption — and that supplementing prostaglandin B1, a nanoplastic-depleted metabolite, partially reversed these effects.
In vitro evaluation of nanoplastics using human lung epithelial cells, microarray analysis and co-culture model
Researchers tested polystyrene nanoplastics on two types of human lung cells and found that the particles caused cell damage, oxidative stress, and inflammation-related gene changes at relatively low concentrations. Using a co-culture model that mimics the lung's layered structure, they showed that nanoplastics can trigger immune responses even in cells not directly exposed. The study suggests that inhaled nanoplastics may pose respiratory health risks through both direct toxicity and inflammatory signaling.
[The effect and mechanism of exposure to polystyrene nanoplastics on lipid metabolism in mice liver].
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.
Nanoplastics Penetrate Human Bronchial Smooth Muscle and Small Airway Epithelial Cells and Affect Mitochondrial Metabolism
When human lung cells were exposed to 25 and 50 nanometer polystyrene nanoplastics in the lab, the particles penetrated both airway lining cells and the smooth muscle cells underneath, including cells from asthmatic donors. The nanoplastics disrupted the cells' energy-producing mitochondria, impairing both normal oxygen-based metabolism and backup energy pathways -- demonstrating a direct mechanism by which inhaled nanoplastics could harm respiratory health.
Polystyrene nanoplastics dysregulate lipid metabolism in murine macrophages in vitro
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.
Airborne polystyrene microplastics and nanoplastics induce nasal and lung microbial dysbiosis in mice
Researchers found that airborne polystyrene microplastics and nanoplastics can induce microbial dysbiosis in the nasal passages and lungs of mice. The study showed that both micro- and nanoplastics altered airway microbiota composition, with microplastics having a stronger influence on lung bacterial communities, suggesting that inhaled plastic particles may disrupt respiratory microbial balance.