Vincent R A, Sheridan R B, Huang P C
Mutat Res. 1975 Dec;33(2-3):357-66. doi: 10.1016/0027-5107(75)90211-0.
Human diploid fibroblast-like cells derived from four patients with the genetic disease ataxia telangiectasia and from two non-mutant donors were examined for the repair of X-ray induced strand breaks in DNA. The ataxia telangiectasia cultures showed no significant differences from the non-mutant cultures in the kinetics and extent of strand repair. This suggests that the increased spontaneous and X-ray induced chromatid aberrations observed in ataxia telangiectasia cells are not caused by a defect in the repair of single strand breaks as might be suspected from a general model of aberration production.
对源自四名患有遗传性疾病共济失调毛细血管扩张症患者以及两名非突变供体的人二倍体成纤维样细胞进行了检测，以研究其对X射线诱导的DNA链断裂的修复情况。在链修复的动力学和程度方面，共济失调毛细血管扩张症细胞培养物与非突变细胞培养物之间未显示出显著差异。这表明，在共济失调毛细血管扩张症细胞中观察到的自发和X射线诱导的染色单体畸变增加，并非如从畸变产生的一般模型中可能推测的那样，由单链断裂修复缺陷所导致。
