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Microbial colonization of microplastics in wastewater accelerates the aging process associated with oxidative stress and the insulin/IGF1 signaling pathway
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Researchers found that microbial colonization of polystyrene microplastics in wastewater accelerates their aging and increases toxicity in organisms, with biofilm-developed microplastics inducing oxidative stress and affecting lifespan through the insulin/IGF1 signaling pathway.
Although polystyrene (PS)-induced toxicity in organisms has been documented, adverse effects on lifespan and molecular mechanisms underlying microbial colonization of PS remain elusive. Herein, physicochemical properties of biofilm-developed PS (B-PS) incubated in wastewater were altered compared with virgin PS (V-PS). Bacterial community adherence to the B-PS surface were also impacted. Acute exposure to V-PS (100 μg/L) and B-PS (10 μg/L) significantly altered the mean lifespan and lipofuscin accumulation of Caenorhabditis elegans, suggesting that B-PS exposure at environmentally relevant concentrations could more severely accelerate the aging process than V-PS. Generation of ROS, gst-4::GFP expression, and oxidative stress-related gene expression were significantly altered following B-PS exposure. Moreover, B-PS exposure increased the nucleus-cytoplasm translocation of DAF-16 and altered the expression of genes encoding the insulin/IGF1 signaling (IIS) pathway. Compared with wild-type nematodes, the daf-16 mutation markedly enhanced lipofuscin accumulation and reduced mean lifespan, whereas daf-2, age-1, pdk-1, and akt-1 mutants could recover lipofuscin accumulation and mean lifespan. Accordingly, B-PS exposure accelerated the aging process associated with oxidative stress and the IIS pathway, and the DAF-2-AGE-1-PDK-1-AKT-1-DAF-16 signaling cascade may play a critical role in regulating the lifespan of C. elegans. This study provides new insights into the potential risks associated with microbial colonization of microplastics.
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Seawater Accelerated the Aging of Polystyrene and Enhanced Its Toxic Effects on Caenorhabditis elegans
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Researchers simulated the aging of polystyrene microplastics in seawater and found that the marine environment accelerated surface erosion, releasing smaller aged particles. When tested on the nematode C. elegans, the aged polystyrene caused greater reductions in movement, vitality, and reproduction compared to virgin particles, driven by increased oxidative stress. The findings suggest that microplastics become more toxic as they weather in ocean conditions.
Sorption processes of wastewater contaminants on virgin and aged polystyrene microplastics: physicochemical changes and cellular toxicity assessment
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Researchers exposed 1 µm polystyrene microplastics (virgin and thermo-oxidation aged) to wastewater and then assessed their adsorption behaviour and cytotoxicity. Aged MPs adsorbed more contaminants from wastewater and showed greater cytotoxicity to human cells than virgin MPs, demonstrating that environmental ageing amplifies the health risks of microplastics.
Microplastic exposure linked to accelerated aging and impaired adipogenesis in fat cells
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Researchers found that microplastic exposure accelerates aging in fat tissue by triggering cellular senescence (a state where cells stop dividing and release inflammatory signals) in both mice and cell cultures. The microplastics accumulated in fat tissue, increased markers of aging and inflammation, and disrupted the normal development of new fat cells. These findings suggest that chronic microplastic exposure could contribute to age-related metabolic problems and obesity-related diseases in humans.
Photoaged Polystyrene Microplastics Accelerate Aging in Caenorhabditis elegans via Ferroptosis-Linked Insulin Signaling Pathway
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Researchers found that photoaged polystyrene microplastics accelerated aging in the nematode C. elegans at environmentally relevant concentrations far more than fresh particles. The aged plastics generated more persistent free radicals and accumulated more readily in the organisms, triggering ferroptosis, a form of iron-dependent cell death, and disrupting insulin signaling pathways. The study suggests that environmental weathering makes microplastics substantially more harmful to biological aging processes.
Polystyrene nanoplastics promotes inflammation and aging in young mice through the oral-gut microbiome axis
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Scientists found that tiny plastic particles (nanoplastics, from the breakdown of everyday plastics) caused young mice to show signs of inflammation and premature aging in their lungs and liver after regular exposure. The likely culprit: these plastics threw off the balance of healthy bacteria in both the mouth and gut, triggering stress and aging signals throughout the body. While this study was done in mice, it raises real concerns about how the plastics we're constantly exposed to might be quietly aging us from the inside out.
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