胚胎期是睾丸生殖细胞分化及发育的关键时期，该时期环境内分泌干扰物（EDCs）暴露可导致生殖细胞尤其是生殖母细胞分化障碍及功能衰退，研究单一或多种EDCs暴露对睾丸生殖细胞的影响及机制具有重要的科学意义。我们前期研究表明，塑化剂邻苯二甲酸酯类化合物DEHP可通过干扰睾酮合成和氧化应激影响睾丸的发育及功能；小剂量植物雌激素染料木黄酮（GEN）可减轻DEHP代谢产物MEHP所致支持细胞氧化损伤，但后一研究仅针对单一的支持细胞成分，未能对睾丸整体及生殖细胞的影响进行评估。本项目拟在前期研究基础上，应用胎鼠睾丸组织离体培养模型（FeTA模型）和现代分子生物学技术，系统研究MEHP与GEN单一或联合暴露对睾丸氧化应激、睾酮合成和生殖细胞分化的影响及其机制，尤其是GEN对MEHP所致睾丸损伤的协同或拮抗（保护）作用及机制，为EDCs暴露风险评估和建立规避方法奠定科学基础，具有重要的理论和实践意义。

The embryonic stage is a critical period for testicular germ cell differentiation and development, endocrine disrupting chemicals (EDCs) exposure during this stage can cause reproductive germ cells, especially the gonocyte differentiation disorder and functional decline, so research on testicular germ cells disruption after single or multiple exposure to EDCs has important scientific and practical significance. Our previous studies had shown that DEHP could disrupt the development and normal function of testes via disrupting testosterone synthesis and oxidative state; low doses of phytoestrogen genistein (GEN) could reduce plasticizer MEHP caused oxidative damage in Sertoli cell , but the study only focuses on single cell component, failing to assess the overall impact of testicular germ cells. This project intends to apply fetal rat testis in vitro culture model (FeTA model ) and use modern molecular biology techniques to study the effects and mechanisms of MEHP / GEN exposure on testicular oxidative stress, testosterone synthesis and germ cells differentiation, and especially clarify the mechanisms involved in the protective role of GEN on MEHP induced testicular damage, which would ultimately provide a tool for EDCs exposure risk assessment and avoidance method, enhancing its important theoretical and practical significance.