The large majority of chromosome damage produced by ionizing radiations takes the form of exchange aberrations. For simple exchanges between two chromosomes, multi-fluor fluorescence in situ hybridization (mFISH) studies confirm that the dose response to X rays or gamma rays is quasilinear with dose. This result is in seeming conflict with generalized theories of radiation action that depend on the interaction of lesions as the source of curvature in dose-response relationships. A qualitative explanation for such “linearization” had been previously proposed but lacked quantitative support. The essence of this explanation is that during the rejoining of radiogenic chromosome breaks, competition for breaks (CFB) between different aberration types often results in formation of complex exchange aberrations at the expense of simple reciprocal exchange events. This process becomes more likely at high radiation doses, where the number of contemporaneous breaks is high and complex exchanges involving multiple breaks become possible. Here we provide mathematical support for this CFB concept under the assumption that the mean and variance for exchange complexity increase with radiation dose.

电离辐射产生的大部分染色体损伤以交换畸变的形式出现。对于两条染色体之间的简单交换，多荧光原位杂交 (mFISH) 研究证实对 X 射线或伽马射线的剂量反应与剂量准线性。这一结果似乎与辐射作用的广义理论相冲突，后者依赖于病变的相互作用作为剂量反应关系中曲率的来源。以前曾提出过对这种“线性化”的定性解释，但缺乏定量支持。这种解释的本质是，在放射性染色体断裂重新连接的过程中，对断裂的竞争（CFB）不同像差类型之间的通常会导致复杂的交换像差的形成，而以牺牲简单的相互交换事件为代价。这个过程在高辐射剂量下变得更有可能，此时同时中断的次数很高，并且涉及多个中断的复杂交换成为可能。在这里，我们在假设交换复杂性的均值和方差随辐射剂量增加的情况下，为该 CFB 概念提供数学支持。