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Papers
8 resultsShowing papers from Ministry of Education
ClearInhalation 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.
Polylactic acid microplastics cause transgenerational reproductive toxicity associated with activation of insulin and hedgehog ligands in C. elegans
Exposure to polylactic acid microplastics -- a supposedly biodegradable plastic -- caused reproductive damage in tiny roundworms that persisted across multiple generations even after the initial exposure ended. The microplastics triggered a chain of genetic changes involving cell death pathways and epigenetic modifications (changes to how genes are read rather than the DNA itself). This transgenerational effect raises concerns that even "green" plastics could have lasting biological consequences.
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.
Polylactic acid microparticles in the range of μg/L reduce reproductive capacity by affecting the gonad development and the germline apoptosis in Caenorhabditis elegans
Researchers exposed C. elegans nematodes to polylactic acid (PLA) microplastics — a supposedly biodegradable plastic — at microgram-per-liter concentrations and found significant reductions in reproductive capacity driven by impaired gonad development and increased programmed cell death (apoptosis) in the germline.
Sentinel supervised lung-on-a-chip: A new environmental toxicology platform for nanoplastic-induced lung injury
Researchers built an advanced lung-on-a-chip device that mimics real lung tissue to study how inhaled nanoplastics cause lung injury. The study found that nanoplastics triggered inflammation and tissue damage patterns similar to chronic obstructive pulmonary disease. This new testing platform could help scientists better understand respiratory risks from airborne plastic particles without relying solely on animal studies.
Unraveling micro/nanoplastics and phthalates in infusion solutions: A novel integrated approach for quantification and cardiovascular cytotoxicity evaluation
Researchers developed a new method to detect and measure micro- and nanoplastics in medical infusion solutions (IV bags) and found significant contamination in commonly used glucose and saline fluids. Nanoplastics dominated the contamination, with polyethylene, polypropylene, and polystyrene detected alongside phthalate chemicals that showed a strong correlation with plastic particle levels. The study suggests that IV therapy may be an overlooked route of direct plastic particle exposure into the bloodstream, and that combined exposure to nanoplastics and phthalates can have synergistic toxic effects on cardiovascular cells.
The hepatotoxicity assessment of micro/nanoplastics: A preliminary study to apply the adverse outcome pathways
Researchers reviewed the literature on how micro- and nanoplastics cause liver damage and organized the findings into an Adverse Outcome Pathway framework. They found that plastic particles can trigger oxidative stress, inflammation, and metabolic disruption in the liver, potentially leading to dysfunction. The study provides a structured way to understand the chain of events from plastic particle exposure to liver harm, highlighting potential health risks for humans.
Activation of p38 MAPK Signaling‐Mediated Endoplasmic Reticulum Unfolded Protein Response by Nanopolystyrene Particles
C. elegans nematodes were exposed to nanopolystyrene at a predicted environmental concentration (1 μg/L) and the study found that p38 MAPK signaling was activated as a protective response, with mutation of the p38 MAPK gene pmk-1 causing increased susceptibility to nanoplastic toxicity through endoplasmic reticulum unfolded protein response. The work reveals a molecular stress response mechanism by which organisms mount a defense against nanoplastic-induced cellular damage.