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Protective role of SIRT1 activation against retinal injury caused by polystyrene micro/nanoplastics exposure
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Tiny plastic particles (the kind found widely in our environment) can build up in eye tissue and damage cells in the retina, the part of your eye responsible for vision, by increasing harmful oxidative stress and speeding up cell aging. Researchers found that boosting a protective protein called SIRT1 with a drug-like activator helped shield retinal cells from this plastic-induced damage in both lab-grown cells and rats. While more research is needed before this becomes a treatment for humans, the study suggests a promising target for protecting eye health as microplastic pollution continues to rise.
Plastic particles are persistent environmental pollutants that can accumulate in ocular tissues and potentially contribute to retinal damage. Sirtuin 1 (SIRT1), a key regulator of oxidative stress and cellular senescence, may play a protective role against plastic-induced retinal injury, but its role remains unclear. In this study, human retinal pigment epithelial (RPE) cells and rat retinas were directly exposed to polystyrene microplastics (PS-MPs, 2 μm) and nanoplastics (PS-NPs, 50 nm), with and without SIRT activator SRT1720. In vitro analyses included cell viability, intracellular reactive oxygen species (ROS), SIRT1 expression, antioxidant enzyme levels (SOD1, SOD2, CAT), and senescence were assessed. In vivo, rats received intravitreal injections of plastic particles, with or without SRT1720 and oxidative stress-related markers, SIRT1 expression, and senescence were evaluated in retinal tissues 7 days after injection. Results showed that PS-MPs and PS-NPs reduced RPE cell viability in a dose- and time-dependent manner, suppressed SIRT1 and antioxidant enzymes, and increased ROS and senescence. PS-NPs induced stronger ROS and senescence than PS-MPs in vitro. Co-treatment with SRT1720 restored SIRT1 expression, improved antioxidant responses, and attenuated ROS and senescence. In vivo, both particle types induced retinal changes similar to those observed in cell experiments. However, there was no significant toxicity difference between PS-MPs and PS-NPs. In conclusion, PS-MPs or PS-NPs promote oxidative stress and senescence in RPE cells and retinal tissue via downregulation of SIRT1 and antioxidant defenses, while SRT1720 provides protective effects. These findings SIRT1 as a potential therapeutic target for plastic-induced retinal injury.
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Tiny plastic particles called nanoplastics—found widely in our environment—can damage the surface of the eye, causing dry eyes and corneal harm, according to a new study in mice and human eye cells. The damage happens because these particles stress out a cell structure that helps proteins fold correctly, triggering inflammation and cell death; promisingly, a drug that relieves this cellular stress reduced the eye damage. While more research is needed to confirm this in humans, the findings raise concerns about how everyday plastic pollution might affect eye health and point to a possible way to protect against it.
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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.
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.
The SIRT gene family protects against oxidative stress and mitochondrial dynamic dysfunction induced by polystyrene nanoplastics in the ovaries of zebrafish (Danio rerio).
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Scientists found that tiny plastic particles (nanoplastics) can damage egg-producing tissue in zebrafish by disrupting a protective protein family called SIRTs, leading to cell stress and lower fertility. Boosting SIRT activity with a natural compound called resveratrol (found in foods like grapes and red wine) helped protect the fish's reproductive health, suggesting a possible way to counteract plastic-related damage. While this study was done in fish, it adds to growing evidence that the microplastics we're all exposed to daily could affect fertility, and hints at potential strategies to protect against it.
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