重离子射线作为放射医学界“新兴、进步”的放疗射线，用于肿瘤放疗具有诸多优势，但对其引起的远后效应了解甚少，尤其是低剂量重离子辐射所致生殖细胞损伤，可诱发的远后期遗传毒性效应。本项目围绕印记基因PEG10和IGF2，拟连续观察（F0-F2代）低剂量重离子辐射（0、0.05、0.1 、0.5 Gy）诱导BALB/c小鼠雄性生殖器官－睾丸印记基因差异表达，印记调控区和启动子区CpG岛的DNA甲基化状态以及印记基因的等位基因表达及亲源表达状态，以早期胚胎发育及胚胎-胎仔发育异常为主要表征，探索低剂量重离子致多代小鼠的遗传毒性效应，并分析生殖细胞中基因印记模式异常与低剂量辐射所致遗传毒性表型间的相关性。旨在探讨印记基因PEG10和IGF2作为低剂量重离子辐射后代遗传风险评估的分子靶标的可行性，并揭示重离子辐照遗传毒理学与印迹基因表观遗传调控的相关机制，补充建立低剂量重离子辐射的表观遗传信息。

Heavy-ion radiotherapy is now recognized as novel, advanced and effective techniques. Despite the many advantages of radiotherapy, the late effects of radiation have not been extensively studied. The project investigates the reproductive and developmental toxicity induced by low-dose heavy ion radiation (0, 0.05,0.1,0.5 Gy) in the continuous passage of BALB/c mice (F0-F2 generation). In view of radiation-induced epigenetic mechanism, the expression of methylated state and location of PEG10 and IGF2 gene,as well as DNA methylation patterns in CpG islands of imprinting control regions and promoters of PEG10 and IGF2 were determined in different generations after radiation. And then we analyze the correlation between aberrant imprinted genes expression or DNA methylation and toxicity phenotypes casused by radiation. The results from the study is possibly permitted to build a available epigenetic mechanism and information related to heavy ion radiation via targeting paternally expressed imprinted gene PEG10 and IGF2.