共济失调毛细血管扩张症淋巴母细胞在辐射暴露后，细胞周期依赖性DNA断裂增加。
Cell cycle dependent DNA break increase in ataxia telangiectasia lymphoblasts after radiation exposure.
作者信息
Humar B, Müller H, Scott R J
机构信息
Research Group Human Genetics, Department of Research, University Clinics, CH-4031 Basel, Switzerland.
出版信息
Mol Pathol. 2001 Oct;54(5):347-50. doi: 10.1136/mp.54.5.347.
The most striking feature of ataxia telangiectasia (AT) cells is their profound sensitivity to ionising radiation. A deficiency in the rejoining of radiation induced DNA breaks has been suggested to be responsible for AT radiosensitivity; however, the existing literature is controversial. A subpopulation, which is present in irradiated AT lymphoblasts, but rarely in controls, has been reported previously. The cells that make up this subpopulation harbour highly fragmented DNA and are responsible for the overall increase in DNA breaks soon after irradiation in AT lymphoblasts. This study examines the influence of the cell cycle on the highly damaged subpopulation. The frequency of highly damaged cells was highest when AT lymphoblasts were irradiated during the G2/M phase. In contrast, AT lymphoblasts irradiated during the G0/G1 phase displayed a frequency similar to control cells. Thus, only G2/M and to some extent S phase cells contribute to an increased DNA break number in AT lymphoblasts early after irradiation. These findings might explain several inconsistencies reported in the literature.
共济失调毛细血管扩张症（AT）细胞最显著的特征是它们对电离辐射极度敏感。有人认为辐射诱导的DNA断裂重新连接缺陷是AT细胞放射敏感性的原因；然而，现有文献存在争议。先前有报道称，在受辐照的AT淋巴母细胞中存在一个亚群，但在对照中很少见。构成这个亚群的细胞含有高度碎片化的DNA，并导致AT淋巴母细胞在辐照后不久DNA断裂总数增加。本研究考察了细胞周期对高度受损亚群的影响。当AT淋巴母细胞在G2/M期受到辐照时，高度受损细胞的频率最高。相比之下，在G0/G1期受到辐照的AT淋巴母细胞显示出与对照细胞相似的频率。因此，只有G2/M期以及在一定程度上S期的细胞会导致AT淋巴母细胞在辐照后早期DNA断裂数量增加。这些发现可能解释了文献中报道的一些不一致之处。
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