Holmberg M, Strausmanis R
Mutat Res. 1983 Apr;120(1):45-50. doi: 10.1016/0165-7992(83)90072-6.
Human lymphocytes were exposed to UV-radiation and X-rays. The previously reported synergistic effect on the frequency of chromosome aberrations (Holmberg and Jonasson, 1974) was measured as a function of the time between the 2 irradiations to study the effect of repair processes in cells in PBS at 20 degrees C. The synergistic effect was found to be rather constant as a function of time (in the interval up to 90 min) when the UV-radiation is delivered first. The synergistic effect decreases with a half-life of about 20 min when the cells are first X-irradiated and after various times are given a UV-treatment. This is not in accordance with findings from dose-fractionation experiments with X-rays, in which lesions interact with each other for several hours. It is proposed that the enhanced aberration frequency in the combined irradiations originates from interactions between short-lived, X-ray-induced DNA-lesions in close spatial proximity (mainly lesions in the same ionization track), and the repair of these lesions are affected by the UV-treatment. In contrast, the aberrations studied in dose-fractionation experiments, by definition, are due to interactions between (long-lived) lesions in different tracks. Further details of this model for aberration production are discussed.
将人类淋巴细胞暴露于紫外线辐射和X射线下。先前报道的对染色体畸变频率的协同效应（Holmberg和Jonasson，1974年）作为两次照射之间时间的函数进行测量，以研究在20摄氏度的PBS中细胞修复过程的影响。当首先进行紫外线辐射时，协同效应作为时间的函数（在长达90分钟的间隔内）相当恒定。当细胞首先接受X射线照射并在不同时间后进行紫外线处理时，协同效应以约20分钟的半衰期下降。这与X射线剂量分割实验的结果不一致，在该实验中，损伤相互作用数小时。有人提出，联合照射中畸变频率的增加源于空间上紧密相邻的短寿命X射线诱导的DNA损伤之间的相互作用（主要是同一电离轨迹中的损伤），并且这些损伤的修复受到紫外线处理的影响。相比之下，剂量分割实验中研究的畸变，根据定义，是由于不同轨迹中（长寿命）损伤之间的相互作用。本文讨论了这种畸变产生模型的进一步细节。
