Molecular and Cellular Biology, Pacific Northwest National Laboratory, Richland, Washington 99354, USA.
Int J Radiat Biol. 2010 Feb;86(2):102-13. doi: 10.3109/09553000903419957.
To investigate radiation-induced bystander responses and to determine the role of gap junction intercellular communication and the radiation environment in propagating this response.
We used medium transfer and targeted irradiation to examine radiation-induced bystander effects in primary human fibroblast (AG01522) and human colon carcinoma (RKO36) cells. We examined the effect of variables such as gap junction intercellular communication, linear energy transfer (LET), and the role of the radiation environment in non-targeted responses. Endpoints included clonogenic survival, micronucleus formation and foci formation at histone 2AX over doses ranging from 10-100 cGy.
The results showed no evidence of a low-LET radiation-induced bystander response for the endpoints of clonogenic survival and induction of DNA damage. Nor did we see evidence of a high-LET, Fe ion radiation (1 GeV/n) induced bystander effect. However, direct comparison for 3.2 MeV alpha-particle exposures showed a statistically significant medium transfer bystander effect for this high-LET radiation.
From our results, it is evident that there are many confounding factors influencing bystander responses as reported in the literature. Our observations reflect the inherent variability in biological systems and the difficulties in extrapolating from in vitro models to radiation risks in humans.
研究辐射诱导的旁观者效应，并确定缝隙连接细胞间通讯和辐射环境在传播这种反应中的作用。
我们使用介质转移和靶向照射来检测原代人成纤维细胞（AG01522）和人结肠癌细胞（RKO36）中的辐射诱导的旁观者效应。我们研究了缝隙连接细胞间通讯、线性能量传递（LET）和辐射环境在非靶向反应中的作用等变量的影响。终点包括克隆存活、微核形成和组蛋白 2AX 焦点形成，剂量范围为 10-100cGy。
结果表明，对于克隆存活和 DNA 损伤诱导等终点，没有低 LET 辐射诱导的旁观者反应的证据。我们也没有看到高 LET、Fe 离子（1GeV/n）辐射诱导的旁观者效应的证据。然而，对于 3.2MeV ɑ 粒子暴露的直接比较显示，这种高 LET 辐射具有统计学上显著的介质转移旁观者效应。
从我们的结果可以明显看出，有许多混杂因素影响旁观者反应，这在文献中有报道。我们的观察反映了生物系统的固有可变性，以及将体外模型推断为人类辐射风险的困难。
