射频（RF）电磁辐射的健康效应备受公众关注，如长期低剂量手机射频辐射（微波频段）可能致白内障。本课题组前期实验表明RF辐射对人晶状体上皮细胞（LECs）产生的氧化损伤可能和线粒体功能受影响有关，并发现RF使线粒体内关键蛋白TFAM表达水平降低。为研究TFAM在RF辐射致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RF辐射LECs模型，利用透射电镜、免疫荧光、核样结构检测等方法全面检测RF辐射下线粒体结构及mtDNA的损伤情况；利用染色质免疫共沉淀、基因调控回复试验等技术首次探讨TFAM在RF辐射致LECs线粒体损伤和mtDNA损伤中的作用及调节机制；利用线粒体提取、免疫共沉淀、关键基因沉默等方法分析RF对TFAM线粒体跨膜转运的影响。本项目预期系统阐明TFAM在RF辐射致LECs线粒体损伤中的作用及调控机制，有望为RF辐射性LECs损伤防治提供理论依据，具有积极的社会意义。

Possible healthy effects induced by radiofrequency fields (RF) radiation have aroused the public concerns, as long-time cell phone RF radiation may cause cataract. Our previous experiments have demonstrated that the oxidative damage in human lens epithelial cells（LECs) induced by RF radiation may be related to the damage of mitochondria and the protein concentration of mitochondrial transcription factor A （TFAM）was decreased in the mitochondria. The aim of this project is to elucidate the role of TFAM in regulation of mitochondria damage after RF radiation in LECs and its underlying mechanism through the established RF radiation LECs model. In present study, the mitochondrial function, structure changes and the mtDNA damage in LECs exposed to1.8 GHz RF will be detected though transmission electron microscopy, respiratory chain assay and nuclear structure assay; the effect of TFAM protein in RF radiation induced mitochondria damage and mtDNA damage will be investigate though ChIP and rescue experiment; the mitochondrial subnormal membrane transport system for TFAM will be detected by mitochondria extract, Co-IP and shRNA. This study will describe the role of TFAM in RF radiation induced mitochondria damage, castlight on the molecular mechanisms of mitochondria’s response to RF radiation, These expected findings will provide new therapeutic strategies for LECs damage by targeting RF radiation, and will be beneficial to the population and communities.