纳米材料对呼吸系统的影响已成为研究纳米材料毒性的关键科学问题。研究表明，纳米SiO2作为应用最广泛的纳米材料，可引起肺脏、睾丸等多脏器的损伤。项目组前期工作发现：纳米SiO2暴露于肺脏、生殖细胞24小时后，细胞凋亡明显增加；成年雄性小鼠暴露于纳米SiO2后，其肺脏、睾丸的组织结构损伤，精子数量降低，Dlk1-Dio3区域中父系表达印记基因上调，IG-DMR区域的DNA甲基化水平降低。但该印记基因区域的具体作用机制以及传代效应是否发生目前尚不清楚。本项目采用小鼠模型，使用生化分析、分子生物学等技术，明确纳米SiO2暴露致肺脏毒性的传代效应的发生。通过动物和细胞实验，应用表观遗传学、生物信息学等方法，阐明Dlk1-Dio3印记区域基因在纳米SiO2致肺脏毒性传代效应中的机制作用。本项目的完成为加强纳米SiO2的防护要求提供理论依据，有效避免纳米SiO2的潜在传代危害，促进人类健康。

As we known, the impact of nanomaterials on the respiratory system has become the key scientific issue for studying the toxicity of nanomaterials. Nano-SiO2 as the most widely used nanomaterials can cause the damage of lung, testis and other organs. After 24 hours of exposure to A549 and GC-1 cells, the cell apoptosis increased significantly. Adult male mice were exposed to nano-SiO2, the structure of lung and testis were damaged, sperm counts decreased, the expression of the Dlk1-Dio3 region imprinted genes were up-regulated and the DNA methylation state of the IG-DMR region decreased. However, it is unclear the mechanism of the Dlk1-Dio3 imprinted region genes and whether the effect would transfer to offspring. To solve these problems, our project used the mouse model, by using the biochemical analysis and molecular biology to ensure the transgenerational effect of nano-SiO2. Through animal and cell experiments, we used epigenetics and bioinformatics methods to elucidated the Dlk1-Dio3 imprinted region genes mediated transgenerational effect induced by nano-SiO2. This project provides the theoretical basis for strengthening the protection requirements, effectively reduced the potential transgenerational damage of nano-SiO2 and promote human health.