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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.
Microplastics (MPs) are known to induce diverse toxic effects across biological systems; however, how environmentally photoaged MPs influence organismal aging and the underlying mechanisms remain poorly understood. Here, virgin polystyrene (PS-0) and 45-day photoaged polystyrene (PS-45) were evaluated at environmentally relevant concentrations (0-100 μg/L) to assess aging-related effects and molecular pathways in Caenorhabditis elegans. Photoaging markedly altered PS physicochemical properties, including surface morphology, crystallinity, and functional groups. Exposure to 100 μg/L PS-0 or PS-45 significantly shortened lifespan, impaired physiological behaviors, and increased lipofuscin accumulation, whereas PS-45 at 10-100 μg/L elicited substantially stronger pro-aging effects. These enhanced toxicities were driven by particle-associated processes, particularly elevated environmentally persistent free radical generation and increased particle accumulation in nematodes. Mechanistically, PS-45 inhibited DAF-16 nuclear translocation and dysregulated insulin/IGF-1 signaling genes (daf-2, age-1, pdk-1, akt-1, and daf-16). Concurrently, PS-45 induced ferroptosis, as evidenced by increased Fe2+ and malondialdehyde levels, glutathione depletion, and suppression of ftn-1; these effects were alleviated by the ferroptosis inhibitor ferrostatin-1. Mutations in daf-2, age-1, pdk-1, akt-1, daf-16, and ftn-1 significantly altered PS-45-induced aging phenotypes and ferroptotic stress, identifying the DAF-2-AGE-1-PDK-1-AKT-DAF-16-FTN-1 axis as a central regulatory pathway. Collectively, this study reveals a mechanistic link between insulin signaling and ferroptosis in MPs-induced aging and highlights the elevated environmental health risks posed by photoaged MPs.
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Researchers exposed the roundworm C. elegans to polystyrene nanoplastics that had been aged by sunlight, simulating real-world environmental conditions. The study found that these weathered nanoplastics caused more severe reproductive harm than pristine particles, primarily through increased oxidative stress, suggesting that aging makes plastic particles more toxic to living organisms.
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Using the tiny roundworm C. elegans, researchers found that combined exposure to nanoplastics and benzo[a]pyrene (a toxic chemical from combustion) at real-world concentrations significantly shortened lifespan and accelerated aging. The pollutant combination disrupted the body's antioxidant defenses, damaged mitochondria, and triggered ferroptosis, a type of cell death involving iron and fat damage. This is concerning because in the real world, microplastics often carry chemicals like this, and their combined effect may be worse than either pollutant alone.
Environmentally persistent free radicals on photoaging microplastics shortens longevity via inducing oxidative stress in Caenorhabditis elegans
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Researchers found that microplastics aged by sunlight develop persistent free radicals on their surface that are more toxic than fresh microplastics. In experiments with a common laboratory worm, these sun-aged microplastics caused significant oxidative stress and shortened lifespan. This is important because most microplastics in the real world have been exposed to sunlight, meaning their actual health risks may be greater than studies using brand-new plastic particles would suggest.
Reproductive toxicity of UV-photodegraded polystyrene microplastics induced by DNA damage-dependent cell apoptosis in Caenorhabditis elegans
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Researchers investigated how UV-photodegraded polystyrene microplastics affect reproduction in the nematode C. elegans at environmentally relevant concentrations. The study found that aged microplastics caused more severe reproductive toxicity than pristine ones, operating through a DNA damage-induced cell death pathway, suggesting that weathered microplastics in the environment may pose greater biological risks.
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.
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