Abstract：
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.
摘要：
塑料污染对生物体的影响已经获得了重要的研究关注。然而,纳米塑料（NPs）对视网膜的影响尚不清楚。本研究旨在探讨聚苯乙烯纳米粒子(PS-NPs)长期暴露对小鼠视网膜的影响。将8周龄的C57BL/6J小鼠在饮用水中暴露于直径为100nm且浓度为10mg/L的PS-NP3个月。PS-NP能够穿透血液视网膜屏障，积聚在视网膜组织，引起氧化应激水平增加，并减少暗视视网膜电反应，而没有明显的结构损伤。PS-NP暴露导致培养的感光细胞的细胞毒性和活性氧积累。PS-NP暴露增加了视网膜色素上皮（RPE）细胞的氧化应激水平，导致基因和蛋白质表达的变化，表明吞噬活性和细胞连接形成受损。长期PS-NP暴露也会加重光诱导的感光细胞变性和视网膜炎症。PS-NP暴露的转录组学谱，光激发的视网膜组织在激活补体介导的吞噬和促炎反应方面与年龄相关性黄斑变性(AMD)患者具有相似的特征.总的来说，这些发现证明了PS-NP对视网膜功能的氧化应激和炎症介导的有害作用，提示长期PS-NP暴露可能是导致视网膜变性的环境危险因素.
