本课题组前期实验表明手机频段微波辐射对人晶状体上皮细胞（LECs）产生氧化介导的线粒体损伤，并首次在高浓度氧化刺激LECs模型中发现硫氧还蛋白2（TXN2）的活性抑制导致线粒体功能障碍并引发细胞凋亡。为研究TXN2在LECs微波辐射后线粒体损伤中的作用并深入探索其机制，本项目拟通过建立的微波辐射LECs线粒体损伤模型，利用Western Blot、过表达质粒载体、干扰RNA、线粒体提取等技术首次探讨TXN2在微波辐射致LECs线粒体损伤和mtDNA损伤中的作用及调节；同时采用RP-HPLC-MS/MS质谱分析及鉴定，寻找受TXN2调控的特异性PSSP，为辐射后线粒体损伤的启动提供解释。本项目预期系统阐明TXN2调控LECs微波辐射后线粒体损伤的机理和分子机制，确定辐射后受TXN2调节线粒体损伤特异性的PSSP。有望为微波辐射性LECs损伤靶向TXN2防治提供理论依据，具有积极的社会意义。

Previous studies have shown that mobile phone radiation induces mitochondria damage by oxidative stress in human lens epithelial cells (LECs). Meanwhile, we have firstly found that the down regulation of thioredoxin 2 (TXN2) activity induced mitochondria dysfunction and apoptosis in LECs after high concentration H2O2 treatment. To elucidate the role of TXN2 in regulation of mitochondria damage after microwave radiation in LECs and its underlying mechanism, this project will use the established microwave radiation induced LECs mitochondria damage model. With helps of Western blot (WB), overexpression plasmid, shRNA and mitochondria extract to investigate the effect of TXN2 protein in microwave radiation induced mitochondria damage and mtDNA damage; Also identify the protein-protein disulfide (PSSP) in TXN2 regulating mitochondria by mass spectrum (MS), and synthesize the TXN2 regulated PSSP by in vitro biochemical assay and evaluate their effects on mitochondria damage. This study will describe the role of TXN2 in microwave radiation induced mitochondria damage, castlight on the molecular mechanisms of mitochondria’s response to microwave radiation, and identify PSSP relating mitochondria. These expected findings will provide new therapeutic strategies for LECs damage by targeting microwave radiation, and will be beneficial to the population and communities.