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Long-term polystyrene nanoparticles exposure reduces electroretinal responses and exacerbates retinal degeneration induced by light exposure
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Researchers found that three months of polystyrene nanoplastic exposure in mice caused particles to penetrate the blood-retinal barrier, accumulate in retinal tissue, generate oxidative stress, and reduce light-sensitivity responses — and that prior nanoplastic exposure significantly worsened light-induced photoreceptor degeneration, with a transcriptomic profile resembling age-related macular degeneration.
The impact of plastic pollution on living organisms have gained significant research attention. However, the effects of nanoplastics (NPs) on retina remain unclear. This study aimed to investigate the effect of long-term polystyrene nanoparticles (PS-NPs) exposure on mouse retina. Eight weeks old C57BL/6 J mice were exposed to PS-NPs at the diameter of 100 nm and concentration of 10 mg/L in drinking water for 3 months. PS-NPs were able to penetrate the blood-retina barrier, accumulated at retinal tissue, caused increased oxidative stress level and reduced scotopic electroretinal responses without remarkable structural damage. PS-NPs exposure caused cytotoxicity and reactive oxygen species accumulation in cultured photoreceptor cell. PS-NPs exposure increased oxidative stress level in retinal pigment epithelial (RPE) cells, leading to changes of gene and protein expression indicative of compromised phagocytic activity and cell junction formation. Long-term PS-NPs exposure also aggravated light-induced photoreceptor cell degeneration and retinal inflammation. The transcriptomic profile of PS-NPs-exposed, light-challenged retinal tissue shared similar features with those of age-related macular degeneration (AMD) patients in the activation of complement-mediated phagocytic and proinflammatory responses. Collectively, these findings demonstrated the oxidative stress- and inflammation-mediated detrimental effect of PS-NPs on retinal function, suggested that long-term PS-NPs exposure could be an environmental risk factor contributing to retinal degeneration.
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In vivo and In vitro assessment of the retinal toxicity of polystyrene nanoplastics
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Researchers found that orally ingested polystyrene nanoplastics can reach the mouse retina within just two hours and, after prolonged exposure, damage the blood-retina barrier, cause oxidative stress, and trigger cell death in retinal tissue. Tests on human retinal cells confirmed similar toxic effects, suggesting that nanoplastic exposure through food and water could pose previously unrecognized risks to eye health.
The toxic effects of polystyrene microplastic/nanoplastic particles on retinal pigment epithelial cells and retinal tissue
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This study found that polystyrene micro and nanoparticles damaged retinal cells in both lab dishes and live mice, causing oxidative stress, mitochondrial dysfunction, and inflammation in the eye. Nanoparticles were able to penetrate into cells and trigger more severe damage than microparticles. With growing use of contact lenses and eye treatments that may introduce plastic particles, these findings raise concerns about microplastic effects on eye health.
Long-term polystyrene nanoplastics exposure aggravates retinal inflammation and photoreceptor degeneration through microglial SPP1 signaling and neutrophil extracellular traps formation
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Scientists found that when mice drank water containing nanoplastics (tiny plastic particles) for two months, it made eye damage from retinal detachment significantly worse by triggering harmful inflammation and immune cell activity in the retina. This matters because it's one of the first studies showing nanoplastics can cross into the eye and worsen a specific eye disease process, adding to growing evidence that everyday plastic pollution may have real consequences for our health beyond just general toxicity.
Short-term PS-NP exposure in early adulthood induces neuronal damage in middle-aged mice via microglia-mediated neuroinflammation
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Researchers orally dosed young mice with polystyrene nanoplastics for one week and observed, ten months later, that particles persisted in brain tissue and drove microglial-mediated neuroinflammation, synapse loss, and cognitive impairment — with minocycline treatment confirming that microglial activation was the key driver of long-term neuronal damage.
Time-dependent effects of polystyrene nanoparticles in brine shrimp Artemia franciscana at physiological, biochemical and molecular levels
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Researchers tracked short- and long-term effects of cationic polystyrene nanoplastics on brine shrimp Artemia, finding that even low concentrations impair growth, trigger cumulative oxidative stress leading to lipid peroxidation, inhibit neural and developmental enzymes including cholinesterase and carboxylesterase, and alter gene expression governing molting and cell protection.
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