环境遗传毒性因素常常会引起DNA损伤。DNA损伤之后决定细胞是生存还是死亡不仅取决于那些能够参与DNA修复、DNA损伤耐受、凋亡和细胞周期检查点的因素，也取于参与自噬的因素。我们在前期研究中发现，HQ能够在肝细胞内诱发DNA损伤反应（DDR）。然而，在HQ诱导肝细胞DNA损伤过程中，自噬与DDR之间关系如何，目前仍不清楚。本研究拟建立氢醌诱导肝细胞自噬实验模型，通过检测细胞自噬状况、细胞形态及活力、细胞凋亡、细胞周期、基因组稳定性、DNA损伤修复能力、DDR相关蛋白及自噬相关蛋白的表达特征、DDR相关蛋白与自噬相关蛋白的相互作用，结合自噬相关信号通路和PIKKs信号通路分析，探讨HQ所致DDR条件下肝细胞自噬与DDR状况之间的定量关系，阐明自噬在HQ致肝细胞DDR过程中的作用及其调控机制，从而为建立机体对HQ所致损伤的防御体系提供科学的理论依据。

Lesions in DNA are frequently caused by environmental and genotoxic agents. The decision between cell survival and death following DNA damage rests on factors that are involved in DNA repair, DNA damage tolerance, apoptosis and cell cycle checkpoints, as well as on factors involved in the activation of autophagy. Our previous studies suggest that hydroquinone can induce DNA damage response(DDR) in hepatocytes. However, the crosstalk between autophagy and DDR in hepatocyte induced by hydroquinone remains unclear. In this study, experimental model of autophagy induced by hydroquinone in hepatocytes will be established. By detecting the status of autophagy, cell morphology and activity, apotosis, cell cycle, genome stability, DNA repair capacity, the epression characteristics of DDR related proteins and autophagy related proteins, the interaction between DDR related proteins and autophagy related proteins, and combined with autophagy related signaling pathway and PIKKs signaling pathway analysis, the quantitative relationship between autophagy and DDR will be explored and the role and its regulatory mechanism of autophagy to DDR induced by hydroquinone in hepatocytes will be elucidated, which will provide scientific theoretical basis to establish the body defense system against the damage caused by hydroquinone.