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Polystyrene nanoplastics and benzo(a)pyrene synergistically induce lung fibrosis and inflammation via relaxin signalling in mice
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Researchers exposed mice to polystyrene nanoplastics, benzo(a)pyrene, or their combination over 16 weeks and found that only combined exposure produced significant lung inflammation and fibrosis, with transcriptomic analysis identifying the Relaxin signaling pathway — acting through PI3K-AKT, MAPK, and calcium-dependent macrophage trap formation — as a key mediator of the synergistic toxicity.
Micro- and nanoplastics (MNPs) are emerging pollutants that can carry harmful substances like benzo(a)pyrene, posing potential health risks. While the harmful effects of nanoplastics on the lungs are known, how they interact with benzo(a)pyrene to affect cellular communication remains unclear. In our study, We explore this interplay using a 16-week mouse model exposed to environmentally relevant doses of polystyrene nanoplastics, benzo(a)pyrene, or a combination of both. We find that only the combined exposure leads to significant lung damage, characterized by severe inflammation and tissue scarring, which are not seen with single exposures. This combined exposure also increases oxidative stress and reduces antioxidant defenses in the lungs. Furthermore, we notice increased levels of inflammation-related molecules and markers of lung tissue damage, confirming a more severe toxic effect. Transcriptomic analysis highlights the involvement of the Relaxin signaling pathway, which influences inflammatory and tissue damage processes through PI3K-AKT and MAPK cascades; Relaxin4 activated PLC-IP3R, opening ER calcium channels and raising cytosolic Ca²⁺, which triggered macrophage extracellular trap (MET) formation. Additionally, a macrophage-MLE-12 co-culture system confirmed that Mix-induced METs are linked to the exacerbation of alveolar inflammation and the progression of pulmonary fibrosis. Our findings reveal novel molecular connections that explain how these pollutants worsen lung health, suggesting that targeting the identified signaling pathways could offer a potential approach to mitigating these harmful effects.
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Synergistic pulmonary toxicity of resorcinol bis(diphenylphosphate) and microplastics: Integrated proteomics and metabolomics approach reveals oxidative stress-inflammatory crosstalk
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Researchers exposed mice to the flame retardant resorcinol bis(diphenylphosphate) alone and in combination with polystyrene nanoplastics through inhalation. Using proteomics and metabolomics analysis, they found that co-exposure produced significantly worse lung damage than the flame retardant alone, through amplified oxidative stress and inflammatory signaling. The study reveals that nanoplastics can intensify the pulmonary toxicity of co-occurring environmental chemicals through synergistic mechanisms.
Co-exposure of polystyrene nanoplastics and ozone synergistically induced airway inflammation: Evidence and biomarkers screening
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Researchers discovered that co-exposure to airborne polystyrene nanoplastics and ozone in mice caused significantly worse airway inflammation than either pollutant alone, with the two acting synergistically. They identified specific metabolic pathways and genes involved in the inflammatory response, providing potential biomarkers for monitoring this type of combined exposure. The findings suggest that breathing in nanoplastics alongside common air pollutants like ozone may pose amplified respiratory health risks.
Combined cytotoxicity of polystyrene nanoplastics and phthalate esters on human lung epithelial A549 cells and its mechanism
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Researchers investigated the combined toxicity of polystyrene nanoplastics and common plasticizer chemicals (phthalate esters) on human lung cells. At lower nanoplastic concentrations, the particles actually reduced the toxicity of the plasticizers by adsorbing them, but at higher concentrations nanoplastics dominated and worsened overall cell damage. The study identified oxidative stress and inflammation as key mechanisms driving the combined toxic effects on lung tissue.
Unveiling the Pulmonary Toxicity of Polystyrene Nanoplastics: A Hierarchical Oxidative Stress Mechanism Driving Acute–Subacute Lung Injury
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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.
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Network toxicology analysis identified 189 potential molecular targets linking polystyrene nanoplastic exposure to lung cancer pathways, and in vitro experiments confirmed that nanoplastics promote lung cancer cell proliferation and resistance to apoptosis via PI3K/AKT signaling.
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