共济失调毛细血管扩张症细胞对博来霉素的反应。
The response of ataxia telangiectasia cells to bleomycin.
作者信息
Lehmann A R, Stevens S
出版信息
Nucleic Acids Res. 1979;6(5):1953-60. doi: 10.1093/nar/6.5.1953.
Abstract
The autosomal recessive disorder, ataxia telangiectasia (AT) is characterised by cellular sensitivity to ionizing radiation. The molecular basis of this radiosensitivity is the subject of controversy. We report here that cultured fibroblasts from AT patients are also sensitive to the lethal effects of bleomycin. As with ionizing radiation, no defect has been observed in the overall rejoining of single or double-strand breaks produced by bleomycin. Since, however, only apyrimidinic (and to a lesser extent apurinic) sites and strand breaks are known to be produced by bleomycin, we tentatively suggest that AT cells are unable to rejoin a very small fraction of the total strand breaks. We attribute our inability to detect such unrejoined strand breaks to the relative insensitivity of the sucrose gradient procedures normally used to detect strand breaks.
摘要
常染色体隐性疾病共济失调毛细血管扩张症（AT）的特点是细胞对电离辐射敏感。这种放射敏感性的分子基础存在争议。我们在此报告，来自AT患者的培养成纤维细胞对博来霉素的致死效应也敏感。与电离辐射一样，未观察到博来霉素产生的单链或双链断裂的总体重新连接存在缺陷。然而，由于已知博来霉素仅产生无嘧啶（以及程度较轻的无嘌呤）位点和链断裂，我们初步认为AT细胞无法重新连接总链断裂中非常小的一部分。我们将无法检测到此类未重新连接的链断裂归因于通常用于检测链断裂的蔗糖梯度程序相对不敏感。
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