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Tracing the cellular consequences of polyethylene microplastics: senescence and apoptosis in A549 and Raw 264.7 macrophage cells
Summary
Researchers exposed human lung epithelial cells (A549) and macrophages (Raw 264.7) to sub-500 nm polyethylene microplastics and found dose-dependent induction of cellular senescence and apoptosis. The results suggest that PE microplastic inhalation could contribute to premature lung cell aging and airway inflammation.
The pervasive accumulation of plastic waste has led to widespread microplastics (MPs) pollution, raising concerns about potential human health impacts. Among these, polyethylene microplastics (PEMPs) are one of the most commonly encountered due to their prevalence in consumer products and the environment. This study investigates the cytotoxic and senescence-inducing effects of PEMPs (≤500 nm) on two cell models, A549 lung epithelial cells and Raw 264.7 macrophages. This study specifically examines cells exposed to varying concentrations of PEMPs (50-500 μg/mL), and key indicators of cellular stress were assessed, including viability, reactive oxygen species (ROS) generation, mitochondrial dysfunction, LDH release, apoptosis, and senescence. Our findings indicate that exposure to PEMPs significantly reduced cell viability and increased ROS production and mitochondrial damage in a dose- and time-dependent manner. At higher concentrations (500 μg/mL), both cell lines demonstrated that PEMPs induce apoptosis and senescence, with A549 cells showing early senescence morphology as early as 24 h post-exposure. These findings confirm the potential of PEMPs to disrupt cellular homeostasis and accelerate aging-related processes. Overall, the study reinforces the urgency of curbing plastic pollution and exploring its association with age-related pathologies and chronic health conditions.
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