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PMMA nanoplastics induce gastric epithelial cellular senescence and cGAS-STING-mediated inflammation via ROS overproduction and NHEJ suppression
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Researchers found that PMMA (acrylic) nanoplastics caused premature aging in stomach lining cells by generating excessive reactive oxygen species and blocking the cells' ability to repair DNA damage. The damaged cells released free DNA fragments that activated inflammatory immune pathways, and mice exposed to the nanoplastics showed behavioral changes associated with aging. This study is notable because most nanoplastic research focuses on polystyrene, and it shows that acrylic nanoplastics can also cause significant harm to the digestive system.
The increasing environmental presence of nanoplastics (NPs) has raised concerns about their potential impact on biological systems. We investigated the repercussions of polymethyl methacrylate (PMMA) NPs exposure on normal gastric epithelial cells and revealed a pronounced increase in senescence-associated β-galactosidase activity and G1 phase cell cycle arrest. Our study demonstrated a dose-dependent increase in reactive oxygen species (ROS) and DNA damage, underscoring the pivotal role of ROS in PMMA NPs-mediated effects, a novel contribution to the existing body of knowledge dominated by polystyrene particles. Furthermore, we explored the influence of PMMA NPs on DNA damage response mechanisms, highlighting the significant inhibition of nonhomologous end-joining (NHEJ). Our findings help to elucidate the consequent genomic instability, as evidenced by increased chromosomal aberrations and micronuclei formation. By connecting these cellular manifestations to organism-level effects, we hypothesize that PMMA NPs play a critical role in aging processes. Our work revealed an activated cGAS-STING signaling pathway after PMMA NPs exposure, which correlated with aging-related inflammation and behavioral changes in mice. Importantly, our study provides comprehensive evidence of PMMA NPs-induced premature aging in gastric epithelial cells, shedding light on the molecular intricacies underlying DNA damage, repair impairment, and inflammation. Our research prompts heightened caution regarding the risks of NPs exposure and calls for further investigation into the broader implications of these environmental pollutants on aging processes in higher organisms.
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Polyvinyl chloride nanoplastics suppress homology-directed repair and promote oxidative stress to induce esophageal epithelial cellular senescence and cGAS-STING-mediated inflammation
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Researchers found that PVC nanoplastics caused premature aging and inflammation in esophageal cells by triggering oxidative stress and blocking the cell's ability to repair DNA damage. The nanoplastics specifically shut down a key DNA repair pathway, leading to genomic instability that activated inflammatory immune signaling. This study identifies the esophagus as a vulnerable organ to nanoplastic damage, which is concerning since the esophagus is directly exposed to plastics swallowed in food and drink.
Polystyrene micro- and nanoplastics induce gastric toxicity through ROS mediated oxidative stress and P62/Keap1/Nrf2 pathway
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In a mouse study, polystyrene micro and nanoplastics at environmentally relevant doses caused significant stomach damage, including reduced gastric juice and mucus production, weakened stomach barrier function, and increased oxidative stress. The damage was driven by reactive oxygen species triggering a specific cell-signaling pathway that led to cell death. This research suggests that microplastics in food and water could harm stomach health, an organ that gets first exposure when contaminated food is consumed.
Effects of micro- and nano-plastics exposure on cellular senescence: an overview.
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Researchers review how micro- and nanoplastics trigger cellular senescence — a state of permanent cell cycle arrest — through oxidative stress and DNA damage, activating pathways like cGAS-STING and NF-κB that elevate risk for age-related diseases, and survey potential therapeutic strategies to counter these effects.
Size-dependent toxicity of polystyrene microplastics on the gastrointestinal tract: Oxidative stress related-DNA damage and potential carcinogenicity
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Researchers found that polystyrene microplastics accumulate mainly in stomach tissue, where smaller nanoscale particles cause more severe damage than larger ones. The nanoplastics reduced antioxidant enzyme activity, increased DNA damage markers, and activated signaling pathways associated with cancer development. These size-dependent effects on the gastrointestinal tract suggest that the smallest plastic particles may pose the greatest risk to digestive health.
Exposure to polystyrene nanoplastics promotes premature cellular senescence through mitochondrial ROS production and dysfunction in pre-differentiated skeletal myoblasts
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This lab study found that polystyrene nanoplastics caused premature aging in muscle precursor cells by damaging their mitochondria and triggering excessive production of harmful molecules called reactive oxygen species. The nanoplastics were absorbed into cells, accumulated there, and caused the cells to stop dividing and show signs of aging. This suggests that nanoplastic exposure could contribute to muscle deterioration and aging-related conditions by damaging the cells responsible for muscle repair.
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