中文摘要：

目的研究乏氧条件下辐射诱导人肝癌细胞HepG2的旁效应及其发生机制。方法采用条件培养基和细胞共培养两种方式，研究细胞在乏氧条件下经X线照射后对未照射旁细胞的影响。结果乏氧可以显著降低细胞的直接辐射损伤效应，即微核的产生。HepG2细胞微核率的氧增比约为1．6。无论是有氧还是乏氧条件下，受辐射细胞均可引起未受照射旁细胞微核率的显著增高，且旁效应程度基本相当，与辐射剂量也存在一定的相关性。另外，活性氧自由基（ROS）清除剂二甲基亚砜（DMSO）和iNOS抑制剂氨基胍（AG）均可显著降低乏氧条件下辐射旁效应引起的细胞微核率，DMSO的降低率为42．2％～46．7％，AG的降低率为42％。结论ROS和NO及其下游信号因子在HepG2细胞乏氧辐射旁效应中具有重要作用。

英文摘要：

Objective To investigate radiation induced bystander effect and its mechanism on hepatoma HepG2 cells under hypoxia condition. Methods Non-irradiated bystander hepatoma cells were co-cultured with irradiated cells or treated with the conditioned medium （CM） from irradiated cells, then micronuclei （MN） were measured for both irradiated cells and bystander cells. Results The MN yield of irradiated HepG2 cells under hypoxic condition was significantly lower than that under normoxia, the oxygen enhancement ratio of HepG2 cells of MN was 1.6. For both hypoxic and normoxic condition, the MN yield of bystander cells were obviously enhanced to a similar high level after co-culturing with irradiated cells or with CM treatment, and it also correlated with the irradiation dose. When the hypoxic HepG2 cells were treated with either DMSO, a scavenger of reactive oxygen species （ROS）, or aminoguanidine, an iNOS inhibitor, the yield of bystander MN was partly diminished, and the reducing rate of DMSO was 42.2 %-46.7 %, the reducing rate of aminoguanidine was 42 %. Conclusion ROS, NO and their downstream signal factors are involved in the radiation induced bystander effect of hypoxic HepG2 cells.