Lebedeva L I, Chubykin V L
Genetika. 1975;11(10):24-9.
20,1% cells with chromosomes aberrations were obtained after UV-irradiation of embryonal fibroblasts of mice at the S-stage in vitro at a decreasing dose of 40erg/mm2. Subsequent gamma-irradiation at the metaphase of the first mitosis at a 5 krad dose led to a statistically significant decrease of the frequency of aberrant cells observed in the same mitosis down to 11,7%. The frequency of spontaneous aberrations did not change during the first few minutes after gamma-irradiation of intact cells at the metaphase. The "protective" effect of gamma-rays can not be explained either by unequal changes of the duration of mitotic stages for aberrant and normal cells, or by sticking of chromosome fragments or by breaks of bridges at the anaphase. The death of cells "under irradiation" also appears to be a hardly probable case of the effect observed. It is assumed that the decrease of the aberrations frequency is the result of predicted earlier modification of the processes of realization of potential chromosome damages into visible aberrations at the metaphase.
在体外对处于S期的小鼠胚胎成纤维细胞以40尔格/平方毫米的递减剂量进行紫外线照射后,获得了20.1%的染色体畸变细胞。随后在第一次有丝分裂中期以5千拉德的剂量进行γ射线照射,导致在同一有丝分裂中观察到的畸变细胞频率在统计学上显著降低至11.7%。在中期对完整细胞进行γ射线照射后的最初几分钟内,自发畸变的频率没有变化。γ射线的“保护”作用既不能用畸变细胞和正常细胞有丝分裂阶段持续时间的不平等变化来解释,也不能用染色体片段的粘连或后期桥的断裂来解释。“受照射”细胞的死亡似乎也不太可能是观察到的这种效应的情况。据推测,畸变频率的降低是先前预测的将潜在染色体损伤在中期转化为可见畸变的过程发生改变的结果。