中文摘要：

采用条件培养基和共培养处理方式，应用微核形成试验研究人神经胶质母细胞瘤T98G细胞，在乏氧条件下经X射线诱导的旁效应及其发生机制。研究发现，乏氧条件下，X射线诱导未照射组细胞的微核率与相应的照射剂量之间存在显著的正相关关系；条件培养基方式下自由基抑制剂二甲基亚砜（Dimethyl sulfoxide，DMSO）可显著降低未照射组细胞的微核率；条件培养基处理乏氧或有氧的T98G细胞，有氧条件培养基处理乏氧细胞引起的旁效应微核率比其它各组均要显著，而诱导型一氧化氮合酶（Inducible nitric oxide syntheses，iNOS）特异性抑制剂氨基胍（Amino guanidine，AG）可抑制条件培养基所诱导的旁效应。推测乏氧条件下，受辐射的T98G细胞所诱导的旁效应与受照射细胞产生的自由基有关，尤其是活性氧自由基和一氧化氮。

英文摘要：

Non-irradiated bystander human glioblastoma T98G cells were co-cultured （CC） with irradiated cells or treated with conditioned medium （CM） from irradiated cells under hypoxic condition, then micronucleus （MN） of both irradiated cells and bystander cells were measured for the investigation of radiation induced bystander effect and its mechanism. It has been found that the MN yield （YMN） of non-irradiated bystander T98G cells is obviously en- hanced after the cell co-culture, or CM treatment, but this increment is diminished by free radical scavenger, dimethyl sulfoxide （DMSO）. When hypoxic or normoxic T98G cells are treated with CM obtained from irradiated cells under either hypoxic or normoxic condition, the biggest bystander response has been observed in the group of hypoxic bystander cells treated with CM from irradiated normoxic cells. However, all of these increments of bystander YMN could be eliminated by aminoguanidine, an iNOS inhibitor. Therefore, under hypoxic condition, free radicals, especiaily reactive oxygen species and nitric oxide, are involved in the bystander response induced by irradiated T98G cells.