Is there a common mechanism underlying genomic instability, bystander effects and other nontargeted effects of exposure to ionizing radiation?
Is there a common mechanism underlying genomic instability, bystander effects and other nontargeted effects of exposure to ionizing radiation?
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DOI：
10.1038/sj.onc.1206992
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发表时间：
2003-10-13
期刊：
影响因子：
8
通讯作者：
Morgan, WF
中科院分区：
文献类型：
--
作者：
Morgan, WF
现在已经描述了一些与辐射暴露相关的非靶向和延迟影响。这些因素包括辐射引起的基因组不稳定、死亡诱导和旁观者效应、碎裂因子和跨代效应。这些非靶向效应不太可能是由细胞辐射直接引起的。相反，有人提出，一些尚未确定的分泌因子可以由辐射细胞产生，可以刺激非辐射细胞的效应(死亡诱导和旁观者效应，碎裂因子)，并在辐射细胞克隆扩增的后代中保持基因组的不稳定性。所提出的因子必须是可溶的，并且能够通过细胞间缝隙连接通信通道在细胞之间传输。此外，它必须具有刺激细胞细胞因子和/或活性氧物种的潜力。虽然很难想象这种分泌因子在跨代效应中的作用，但辐射的其他非靶向效应可能都有一个共同的机制。
A number of nontargeted and delayed effects associated with radiation exposure have now been described. These include radiation-induced genomic instability, death-inducing and bystander effects, clastogenic factors and transgenerational effects. It is unlikely that these nontargeted effects are directly induced by cellular irradiation. Instead, it is proposed that some as yet to be identified secreted factor can be produced by irradiated cells that can stimulate effects in nonirradiated cells (death-inducing and bystander effects, clastogenic factors) and perpetuate genomic instability in the clonally expanded progeny of an irradiated cell. The proposed factor must be soluble and capable of being transported between cells by cell-to-cell gap junction communication channels. Furthermore, it must have the potential to stimulate cellular cytokines and/or reactive oxygen species. While it is difficult to imagine a role for such a secreted factor in contributing to transgenerational effects, the other nontargeted effects of radiation may all share a common mechanism.