重离子引起的早熟性衰老是非常重要的辐射损伤效应，能使细胞生长停止、功能发生退化性改变，但相关研究却非常有限。前期工作中我们新发现并首次报道了碳离子辐射引起黑色素瘤92-1细胞早熟性衰老与细胞周期停顿有关。本项目拟用兰州重离子加速器产生的多种重离子验证周期停顿在92-1细胞中发生的普遍性，通过研究CyclinB1、CyclinD1等与周期和衰老密切相关的蛋白表达变化，探明细胞周期停顿在早熟性衰老中的关键作用，最后通过不同辐照剂量下G2期细胞比率、CyclinB1表达量随时间变化的动力学，获得与周期停顿相关的衰老发生的剂量阈值。该项目具有良好的基础，完成以后极有可能在衰老新机制方面获得突破性进展，不仅能给传统放射生物学新热点的探讨提供有价值的学术资料，而且符合当前国际国内肿瘤治疗和太空辐射风险评估中对深化重离子辐射生物效应研究的迫切需求。

The premature senescence induced by heavy ions is a very important radiobiological effect. It causes inhibition of cell growth and reduction of cellular function. However, researches in this field are very limited. In our previous work, we found and reported for the first time that premature senescence is related to cell cycle suspension induced by carbon beam on a melanoma cell line 92-1. In this study, 92-1 cells are going to be irradiated with beams produced by the accelerator in Lanzhou. The cell cycle suspension will be verified with different kinds of heavy ions. The expression level of proteins which play important roles in cell cycle and senescence, such as CyclinB1 and CyclinD1, will be checked. The mechanisms of cell cycle suspension in premature senescence will be identified. The time kinetics of G2 cells and CyclinB1 with different doses will be found out to obtain the dose threshold of cell cycle suspension related senescence. Based on the data we have obtained, it is very promising to achieve notably results on the mechanisms involved in senescence. These studies not only enrich the knowledge of traditional radiobiology, but also provide useful reference data for the heavy ion therapy and the risk estimation of heavy ion radiation in space.