Scott D, Zampetti-Bosseler F
Int J Radiat Biol Relat Stud Phys Chem Med. 1982 Dec;42(6):679-83. doi: 10.1080/09553008214551661.
The delay in progression of X-irradiated cells through the cell cycle, which is more pronounced in normal (N) than in A-T fibroblasts, is greatest for cells in G2 at the time of irradiation. The greater effect of radiation on the initiation of DNA synthesis in N than in A-T cells is reflected in the shape of the percent labelled mitosis curves after 3H-thymidine treatment. The duration of the S phase in unirradiated A-T cells is greater than in N cells. Any explanation of the underlying defect in A-T must account not only for the reduced radiosensitivity of DNA synthesis but for the lesser delay in G2. Our data support the hypothesis that DNA is the principal target for radiation-induced G2 delay.
经X射线照射的细胞在细胞周期进程中的延迟,在正常(N)成纤维细胞中比在共济失调毛细血管扩张症(A-T)成纤维细胞中更明显,且在照射时对处于G2期的细胞影响最大。辐射对N细胞中DNA合成起始的影响比对A-T细胞的影响更大,这反映在3H-胸腺嘧啶处理后的标记有丝分裂曲线百分比的形状上。未照射的A-T细胞中S期的持续时间比N细胞中的长。对A-T潜在缺陷的任何解释不仅必须说明DNA合成放射敏感性的降低,还要说明G2期延迟较小的原因。我们的数据支持DNA是辐射诱导G2期延迟的主要靶点这一假说。