聚苯乙烯纳米塑料暴露引发小鼠角膜氧化应激与线粒体依赖性凋亡  

Polystyrene nanoplastics exposure induces oxidative stress and mitochondria-dependent apoptosis in mouse corneas

作　　者：王立言 赵晗竹 魏超 苏欣然 李玮[2] 刘尚明 Wang Liyan;Zhao Hanzhu;Wei Chao;Su Xinran;Li Wei;Liu Shangming(The Laboratory Center for Basic Medicine,School of Basic Medical Sciences,Shandong University,Jinan 250012,China;Biomedical Engineering Institute,School of Control Science and Engineering,Shandong University,Jinan 250061;Department of Pathology,Jinan Maternal and Child Health Hospital,Jinan 250001)

机构地区：[1]山东大学基础医学院基础医学实验中心,济南250012 [2]山东大学控制科学与工程学院生物医学工程研究所,济南250061 [3]济南市妇幼保健院病理科,济南250001

出　　处：《中国组织化学与细胞化学杂志》2025年第1期27-32,共6页Chinese Journal of Histochemistry and Cytochemistry

基　　金：国家自然科学基金(22176115)。

摘　　要：目的本研究旨在评估聚苯乙烯纳米塑料(polystyrene nanoplastics,PSNPs)暴露对小鼠角膜多层组织的急性毒性效应,重点探讨氧化应激和线粒体依赖性凋亡的机制。方法采用滴眼暴露法,将小鼠角膜暴露于200μg/mL浓度的PSNPs悬液,持续8 d。通过TUNEL染色、透射电子显微镜(TEM)观察、Western blot检测及生化指标检测分析,评估PSNPs对角膜组织的毒性效应及其机制。结果PSNPs暴露显著增加角膜组织中的丙二醛(MDA)水平,表明氧化应激加剧;总抗氧化能力(T-AOC)显著下降,提示抗氧化防御功能受损。TUNEL染色结果显示,角膜各层组织细胞的凋亡比例显著增加,尤其在上皮层。透射电子显微镜观察到,暴露组角膜上皮层、基质层和内皮层均存在不同程度的线粒体损伤,表现为线粒体肿胀、嵴结构破坏等典型病变。Western blot分析发现,PSNPs暴露后促炎因子TNF-α的表达略有上调,但未达显著差异。结论PSNPs暴露通过引发氧化应激,导致角膜各层组织的线粒体损伤和细胞凋亡,表现出层次性毒性特征。该研究揭示了PSNPs对角膜的急性毒性机制,特别是氧化应激驱动的线粒体依赖性凋亡通路,为微塑料污染的眼部健康风险评估提供了新的数据支持。Objective This study aimed to evaluate the acute toxic effects of polystyrene nanoplastics(PSNPs)exposure on the multi-layered tissues of the mouse cornea,with a focus on the mechanisms of oxidative stress and mitochondria-dependent apoptosis.Methods The mouse cornea was exposed to a 200μg/mL concentration of PSNPs suspension via eye drop administration for 8 days.The toxic effects and mechanisms of PSNPs on corneal tissues were assessed using TUNEL staining,transmission electron microscopy(TEM),Western blot analysis,and biochemical assays.Results PSNPs exposure significantly increased malondialdehyde(MDA)levels in corneal tissues,indicating aggravated oxidative stress.Total antioxidant capacity(T-AOC)was significantly reduced,suggesting impaired antioxidant defense.TUNEL staining revealed a significant increase in apoptosis in all layers of corneal tissue,particularly in the epithelial layer.TEM observations showed varying degrees of mitochondrial damage in the epithelial,stromal,and endothelial layers of the cornea in the exposed group,characterized by mitochondrial swelling and cristae structure disruption.Western blot analysis indicated a slight upregulation of the pro-inflammatory factor TNF-αafter PSNPs exposure,but the difference was not statistically significant.Conclusion PSNPs exposure induces oxidative stress,leading to mitochondrial damage and apoptosis in all layers of the cornea,demonstrating a hierarchical toxic effect.This study reveals the acute toxic mechanisms of PSNPs on the cornea,particularly the oxidative stress-driven mitochondria-dependent apoptosis pathway,providing new data for assessing the ocular health risks of microplastic pollution.

关 键 词：聚苯乙烯纳米塑料 角膜 氧化应激 细胞凋亡 多层组织 

分 类 号：R772.2[医药卫生—眼科]