以污染严重、暴露广泛、危害大的壬基酚为受试物，以壬基酚致FSH等紊乱和睾丸生精功能损害为切入点，以FSH能通过MAPK-ERK、PI3K/Akt、LKB1/AMPK等途径调控睾丸支持细胞mTORC1信号通路为依据，以壬基酚对mTORC1信号转导通路的影响为主线，以揭示其对mTORC1信号通路的影响及其对睾丸生精功能损害的分子机制为目标。采用先进的分子生物学技术，在动物、细胞和分子水平上，重点研究大鼠睾丸组织中mTORC1信号转导通路在壬基酚致睾丸生精损害中的作用及其与支持细胞和生精细胞凋亡之间的关系，找出壬基酚对mTORC1信号通路上、下游作用的关键环节和靶标，揭示在壬基酚作用下睾丸组织 中mTORC1信号通路各环节之间的相互作用及其与睾丸支持细胞和生精细胞凋亡间的内在联系，从mTORC1信号通路角度阐释壬基酚致睾丸生精功能障碍的分子机制，为制定壬基酚致男性生殖危害的防制提供新的学术思路。

Nonylphenol is a widespread and dangerous pollutant. In order to elucidate effects of nonylphenol on mTORC1 pathway and discover mechanisms by which nonylphenol injures testicular spermatogenic function, this study regards the disorder of FSH and injury of testicular spermatogenic function as entry points, considers that FSH regulates mTORC1 pathway of sertoli cells via MAPK-ERK, PI3K/Akt, LKB1/AMPK, etc. as basis, and treats effects of nonylphenol on mTORC1 pathway as principal clue. Various advanced biomolecular techniques will be used on levels of animals, cells and molecules to study functions of mTORC1 pathway in nonylphenol-induced injury of testicular spermatogenic function, find key links and effect targets in the pathway, and reveal their interactions and inner links. To illuminate mechanisms by which nonylphenol results in the disorder of testicular spermatogenic function from the angle of mTORC1 pathway, will provide new insights into prevention of nonylphenol-induced injury of male reproduction.