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Polystyrene nanoplastics induce ocular surface toxicity via endoplasmic reticulum stress
Summary
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.
The increasing environmental burden of micro/nanoplastics (M/NPs) has heightened concerns about their potential threat to ocular health, yet the molecular mechanisms underlying M/NPs-induced ocular surface injury remain largely unclear. In this study, we investigated the ocular toxicity of polystyrene nanoplastics (PS-NPs) with a focus on the involvement of endoplasmic reticulum (ER) stress. A mouse ocular exposure model and a human corneal epithelial (HCE-T) cell model were established. Multi-level analyses demonstrated that PS-NPs exposure induced ocular surface toxicity in mice, characterized by diminished tear secretion and corneal epithelial damage. At the cellular level, PS-NPs were internalized by HCE-T cells and accumulated near the ER. Mechanistic investigations revealed that PS-NPs exposure was associated with the activation of the ER stress response, which was accompanied by disrupted redox homeostasis, NF-κB-driven inflammatory activation, promoted apoptosis, and impaired epithelial barrier integrity. Notably, administration of the chemical chaperone 4-phenylbutyric acid (4-PBA), an ER stress inhibitor, substantially attenuated these adverse outcomes in vivo and in vitro. Together, this study establishes a significant association between PS-NPs exposure, ER stress activation, and ocular damage, identifying ER stress as a key and targetable cellular event in the toxicological response to NPs.