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61,005 resultsShowing papers similar to Characterisation of changes in global genes expression in the lung of ICR mice in response to the inflammation and fibrosis induced by polystyrene nanoplastics inhalation
ClearDynamic 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.
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.
Polystyrene nanoplastics induced lung injury in mice: Insights into lung metabolic disorders
Researchers exposed mice to polystyrene nanoplastics through the airway and found that the particles caused lung inflammation and tissue damage. Using metabolomics analysis, they discovered that the nanoplastics disrupted multiple metabolic pathways in lung tissue, with surface-modified particles causing more severe effects. The study provides evidence that inhaled nanoplastics can alter lung metabolism in ways that may contribute to respiratory health problems.
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.
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.
Effects of Atmospheric Aging on the Respiratory Toxicityof Polystyrene Nanoplastic Particles
Researchers exposed human bronchial epithelial cells to atmospherically aged polystyrene nanoplastics at an air-liquid interface, finding significantly elevated expression of inflammatory genes IL-8, TNF-α, and IL-6 compared to fresh nanoplastics, demonstrating that environmental aging increases respiratory toxicity.
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.
Nasal instillation of polystyrene nanoplastics induce lung injury via mitochondrial DNA release and activation of the cyclic GMP-AMP synthase-stimulator of interferon genes-signaling cascade
Researchers showed that inhaled polystyrene nanoplastics trigger lung fibrosis and inflammation in mice by inducing mitochondrial DNA release into the cytoplasm, which activates the cGAS-STING innate immune signaling pathway — a discovery that identifies a specific molecular mechanism linking nanoplastic inhalation to pulmonary injury.
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.
Deleterious effects of microplastics and nanoplastics on rodent lungs: a systematic review
This systematic review summarizes research on how inhaled micro- and nanoplastics affect the lungs in animal studies. The findings show these particles can cause lung inflammation, tissue damage, and immune responses, suggesting that breathing in airborne microplastics may pose real risks to respiratory health.
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.
Acute exposure to polystyrene nanoplastics induces unfolded protein response and global protein ubiquitination in lungs of mice
Mice exposed to polystyrene nanoplastics through their airways showed signs of cellular stress in lung tissue, including activation of the unfolded protein response (a defense mechanism cells use when proteins are damaged) and increased protein breakdown. The effects were dose-dependent, with higher nanoplastic doses causing more cellular distress. This research reveals a specific mechanism by which inhaled nanoplastics could damage lung cells, raising concerns about airborne microplastic exposure.
Polystyrene nanoplastics induce pulmonary oxidative stress and programmed cell death through the cGAS-STING-NLRP3 pathway
Researchers exposed mice to polystyrene nanoplastics through nasal administration and studied the resulting lung damage over seven days. They found that the nanoplastics triggered oxidative stress, programmed cell death, and inflammatory responses in lung tissue through activation of the cGAS-STING-NLRP3 signaling pathway. The study provides evidence that inhaled nanoplastics can cause acute lung injury through specific molecular mechanisms involving both apoptosis and pyroptosis.
Unveiling the systemic impact of airborne microplastics: Integrating breathomics and machine learning with dual-tissue transcriptomics
Researchers developed a new non-invasive way to detect microplastic damage in mice by analyzing chemicals in their breath. When mice inhaled tiny polystyrene particles, the plastics caused inflammation in their lungs and injury to their hearts, with specific breath chemicals serving as warning signs. This approach could eventually help doctors detect microplastic-related health problems in people through a simple breath test.
Effects of Atmospheric Aging on the Respiratory Toxicity of Polystyrene Nanoplastic Particles
Researchers exposed human bronchial epithelial cells to atmospherically aged polystyrene nanoplastics at an air-liquid interface, finding that oxidized particles significantly elevated inflammatory gene expression (IL-8, TNF-α, IL-6) compared to fresh particles, demonstrating that environmental aging enhances respiratory toxicity.
Oropharyngeal Administration of Polystyrene Microplastics Induces Profibrotic and Oxidative Changes in Murine Lung Tissue
Researchers investigated the early lung effects of inhaled polystyrene microplastics in mice over a 21-day exposure period. While overall fibrosis scores did not reach statistical significance in this short timeframe, they observed significant macrophage infiltration, active particle uptake by immune cells, and upregulation of oxidative stress and fibrosis-related molecular markers. The findings suggest that microplastic inhalation triggers early immune and oxidative responses that may precede lung tissue remodeling.
Polystyrene Nanoplastics Induce Lung Injury via Activating Oxidative Stress: Molecular Insights from Bioinformatics Analysis
Researchers found that polystyrene nanoplastics induce lung cell injury through oxidative stress pathways, identifying key transcription factors and the molecule TNFRSF12A as crucial mediators of nanoplastic-triggered redox imbalance and respiratory damage.
Integrated 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.
In vivo toxicity assessment of microplastics in Balb/C mice : study of inhalation exposure and its inflammatory effects
Researchers examined the in vivo toxicity of inhaled microplastics in Balb/C mice, studying pulmonary inflammation, oxidative stress, and systemic effects following repeated inhalation exposure. The study found dose-dependent lung inflammation and evidence of particle translocation to other organs.
Unmodified Polystyrene Nanoparticles Induce Inflammatory and Oxidative Stress Responses in Human Lung Epithelial Cells
Exposure of human lung epithelial cells to unmodified polystyrene nanoparticles (60 nm) at concentrations as low as 50 µg/mL reduced cell viability by about 50% and triggered expression of inflammatory genes including IL-6 and CXCL10. These results suggest that nanoplastic particles reaching the respiratory tract could provoke lung inflammation, raising concerns about the health consequences of inhaling airborne nanoplastics.
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.
Gender-specific effects of prenatal polystyrene nanoparticle exposure on offspring lung development
Researchers found that prenatal exposure to polystyrene nanoparticles impairs lung development in mouse offspring in sex-specific ways — females showed inflammation and disrupted surfactant proteins while males had impaired blood vessel growth — both increasing the risk of a serious lung condition called bronchopulmonary dysplasia.
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.
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.