邻苯二甲酸单(2-乙基己基)酯（MEHP）可通过过量活性氧簇（ROS）的产生诱导睾丸发生氧化应激，造成生精细胞损伤和凋亡。申请者前期研究发现抗氧化蛋白Prx2在输精管结扎后的小鼠睾丸中表达显著上调，缓解了睾丸的氧化损伤，这预示着其在保护生精细胞方面的重要作用。但仍有以下问题需要研究：（1）细胞内的Prx2基因在生精细胞氧化损伤过程中的功能及分子机制；（2）生精细胞损伤时Prx2是否会发生移位。本课题拟在前期工作的基础上，以上述两点为切入点，揭示细胞内Prx2对MEHP致小鼠精母细胞氧化损伤的保护机制。通过本项目研究可为防治邻苯二甲酸酯类造成的男性生殖功能损伤提供新的思路和靶点。

Mono-(2-ethylhexyl) Phthalate (MEHP) can induce oxidative stress in testis through the overproduction of ROS, which could lead to the damage and apoptosis of spermatogenic cells. The results of our previous study showed that the expression of Prx2 was significantly up-regulated in vasectomized testis, subsequently ameliorating testicular damage towards control level, which implied the important role of Prx2 in protecting spermatogenic cells from oxidative damage. However, there were still the following problems need to be studied: (1) the function and molecular mechanism of intracellular Prx2 gene in spermatogenic cells damage caused by oxidative stress, (2) the subcellular localization of Prx2 when spermatogenic cells oxidative injury. Based on our previous work, we will reveal the protection mechanism of Prx2 on mouse spermatocyte-derived cell line damage induced by MEHP from the above two points in the present study. This project will provide new ideas and drug targets for the prevention and cure the damage of male reproductive function induced by phthalate esters.