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61,005 resultsShowing papers similar to Acute exposure to polystyrene nanoplastics induces unfolded protein response and global protein ubiquitination in lungs of mice
ClearExposure 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.
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 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.
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.
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 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.
Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line
A cell study found that polystyrene nanoplastics cause dose-dependent damage to human lung cells, triggering oxidative stress, premature cell aging, and cell death. These findings suggest that breathing in nanoplastics could harm lung tissue over time and potentially contribute to cancer risk from air pollution.
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.
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 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.
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.
Polystyrene-nanoplastics-induced unfolded protein response in monocyte-derived macrophages mediates pulmonary fibrosis via oxidative-stress-dependent IL-6 secretion
Researchers found that inhaled polystyrene nanoplastics promote pulmonary fibrosis by activating macrophages through a PERK/oxidative stress/IL-6 signaling cascade — in which nanoplastics trigger an unfolded protein response (a cellular stress reaction) that drives IL-6 secretion and transforms fibroblasts into scar-forming cells — identifying IL-6 as a potential therapeutic target.
Endoplasmic reticulum stress-induced NLRP3 inflammasome activation as a novel mechanism of polystyrene microplastics (PS-MPs)-induced pulmonary inflammation in chickens
Researchers exposed chickens to polystyrene microplastics for 42 days and found significant lung damage, including tissue inflammation and cell stress responses. The microplastics triggered a chain reaction starting with stress in the endoplasmic reticulum (a cell structure involved in protein processing) that activated inflammatory pathways. While this study focused on poultry, similar inflammatory mechanisms could be relevant to understanding how microplastics affect lungs in other species, including humans.
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.
Intratracheal Administration of Polystyrene Micro(nano)plastics with a Mixed Particle Size Promote Pulmonary Fibrosis in Rats by Activating TGF-β1 Signaling and Destabilizing Mitochondrial Dynamics and Mitophagy in a Dose- and Time-Dependent Manner.
SD rats exposed to mixed polystyrene micro(nano)plastics via intratracheal administration at escalating doses over time developed pulmonary fibrosis and mitochondrial dysfunction, with severity linked to dose. The findings demonstrated a clear biological pathway connecting inhaled microplastic exposure to lung injury.
Investigation of pulmonary toxicity evaluation on mice exposed to polystyrene nanoplastics: The potential protective role of the antioxidant N-acetylcysteine
Researchers investigated lung damage in mice exposed to inhaled polystyrene nanoplastics and tested whether the antioxidant N-acetylcysteine could offer protection. They found that nanoplastics caused significant lung inflammation, tissue damage, and oxidative stress, but N-acetylcysteine treatment helped reduce these harmful effects. The study suggests that oxidative stress is a key mechanism behind nanoplastic-induced lung injury and points to potential protective strategies.
Size-dependent toxicity of polystyrene microplastics in lung cells: An in vivo and in vitro study
Researchers investigated the size-dependent toxicity of polystyrene microplastics in lung cells using both mouse and cell culture models. The study found that smaller 1-micrometer particles accumulated more in lung tissue than larger particles and identified epithelial-mesenchymal transition as a key toxic mechanism, driven by ECM-MMP signaling cascades that contribute to lung injury.
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.
Polystyrene nanoplastics aggravate house dust mite induced allergic airway inflammation through EGFR/ERK-dependent lung epithelial barrier dysfunction
In mice with allergic asthma triggered by house dust mites, exposure to polystyrene nanoplastics significantly worsened airway inflammation and lung damage. The nanoplastics disrupted the protective barrier of lung cells by activating a specific signaling pathway (EGFR/ERK), allowing more allergens and immune cells to penetrate lung tissue. This finding suggests that airborne nanoplastics could make asthma and allergies worse for the millions of people who already suffer from these conditions.
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.
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.
Uptake of Breathable Nano- and Micro-Sized Polystyrene Particles: Comparison of Virgin and Oxidised nPS/mPS in Human Alveolar Cells
Researchers found that environmentally aged (oxidised) nano- and microplastics were rapidly taken up by human lung cells and caused significantly greater DNA damage, oxidative stress, and mitochondrial impairment compared to pristine particles, highlighting the heightened health risks of weathered airborne plastics.
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
Researchers exposed mice to inhaled polystyrene nanoplastics for two weeks and used microarray analysis to identify 115 differentially expressed lung genes, with inflammation and fibrosis pathways significantly upregulated — findings that propose specific gene biomarkers for monitoring nanoplastic-induced pulmonary damage.
Size-Dependent PulmonaryToxicity and Whole-Body Distributionof Inhaled Micro/Nanoplastic Particles in Male Mice from Chronic Exposure
Researchers used a whole-body inhalation exposure system to chronically expose male mice to polystyrene micro- and nanoplastics at environmental concentrations and tracked particle distribution and lung toxicity. Nanoplastics (80 nm) showed greater tissue transport than microplastics (1 µm), with highest accumulation in lungs followed by blood and spleen, and both sizes disrupted oxidative balance and antioxidant defenses.