目的探索细胞间隙通讯(GJIC)对重离子辐射细胞效应的影响及其机制。方法受到不同试剂处理的AG1522细胞和HSG细胞在高能碳离子束辐照后,检测其细胞损伤。结果重离子辐照对细胞产生致死性损伤、细胞周期的阻滞,且AG1522比HSG具有更高的辐射敏感性。对AG1522细胞单层,GJIC可以正向调控辐射损伤。但对HSG细胞单层,受到增强的GJIC则对细胞具有辐射保护作用。另外,DMSO降低了AG1522细胞的微核率,但PTIO可增强HSG的微核率。结论GJIC对正常母细胞和肿瘤细胞的辐射损伤具有不同的作用,ROS和NO是其中重要的信号因子。
Objective To investigate the influence of GJIC on heavy-ion irradiation induced cellular damage and associated mechanism. Methods Primary human fibroblast AG1522 and human neoplastic HSG cells under confluence were irradiated with high-energy carbon beam. The influence of gap junctional intercellular communication (GJIC) on radiation responses of micronucleus (MN) formation and cycle arrest was measured. Results Cell lethal damage and cell cycle arrest were induced by high energy carbon beam, and AG1522 cells had radiosensitivity higher than HSG ceils. For irradiated AG1522, cellular damage was positively adjusted by GJIC. However, with respect to irradiated HSG cells, cell damage was diminished by enhanced GJIC. Moreover, MN in AG1522 was reduced by DMSO and MN in HSG cells was increased by PTIO. Conclusions GJIC increases radiation damage on primary fibroblasts but has radiation protective effect on tumor cells. ROS and NO may contribute to these GJIC mediated radiation responses on AG1522 and HSG cells, respectively.