Barnard Stephen, Bouffler Simon, Rothkamm Kai
Health Protection Agency Centre for Radiation, Chemical and Environmental Hazards, Chilton, Didcot, Oxon OX11 0RQ, UK.
Genome Integr. 2013 Mar 22;4(1):1. doi: 10.1186/2041-9414-4-1.
DNA double-strand breaks are among the most deleterious lesions induced by ionising radiation. A range of inter-connected cellular response mechanisms has evolved to enable their efficient repair and thus protect the cell from the harmful consequences of un- or mis-repaired breaks which may include early effects such as cell killing and associated acute toxicities and late effects such as cancer. A number of studies suggest that the induction and repair of double-strand breaks may not always occur linearly with ionising radiation dose. Here we have aimed to identify and discuss some of the biological and methodological factors that can potentially modify the shape of the dose response curve obtained for these endpoints using the most common assays for double-strand breaks, pulsed-field gel electrophoresis and microscopic scoring of radiation-induced foci.
DNA双链断裂是电离辐射诱导产生的最具危害性的损伤之一。一系列相互关联的细胞反应机制已经进化出来,以实现对其的高效修复,从而保护细胞免受未修复或错误修复的断裂所带来的有害后果,这些后果可能包括早期效应,如细胞死亡及相关的急性毒性,以及晚期效应,如癌症。多项研究表明,双链断裂的诱导和修复可能并不总是与电离辐射剂量呈线性关系。在此,我们旨在识别和讨论一些生物学和方法学因素,这些因素可能会改变使用双链断裂最常用检测方法(脉冲场凝胶电泳和辐射诱导灶的显微镜评分)获得的这些终点剂量反应曲线的形状。