Mothersill C, Seymour C B
Radiation Science Centre, Dublin Institute of Technology, Ireland.
Mutagenesis. 1998 Sep;13(5):421-6. doi: 10.1093/mutage/13.5.421.
Recently there has been considerable interest in various delayed effects of radiation. These have the common property of showing a high and, in some instances, non-clonal transmission of 'damage' to distant progeny which derive from apparently normal surviving cells and their descendants. This means that conventional analysis and interpretation of long-term radiation damage in terms of mutations induced in DNA at the time of radiation exposure may be incorrect. Several reviews of this area have appeared in recent years which have described the historical development of this field. The aim of this commentary is to highlight areas of discussion, particularly concerning links between the various end-points, and to discuss some of the possible implications of genomic instability for radiation carcinogenesis in general and for the setting of radiation protection action limits in particular.
最近，人们对辐射的各种延迟效应产生了浓厚兴趣。这些效应具有一个共同特性，即对源自明显正常存活细胞及其后代的远处子代显示出高度且在某些情况下非克隆性的“损伤”传递。这意味着，依据辐射暴露时DNA中诱导的突变对长期辐射损伤进行的传统分析和解释可能是不正确的。近年来，该领域出现了几篇综述，描述了这一领域的历史发展。本评论的目的是突出讨论的领域，特别是关于各种终点之间的联系，并讨论基因组不稳定对一般辐射致癌作用以及特别是对辐射防护行动限值设定的一些可能影响。
