Barenfel'd L S, Nergadze S G, Pleskach N M, Mikhel'son V M
Tsitologiia. 1994;36(7):680-6.
Using DNA fiber autoradiography, DNA replication in cultured fibroblasts, derived from normal donors, and from XPII patient with increased sensitivity to ionizing radiation was estimated. Here evidence is provided on the fact that the fork movement, significantly decreased in XPII cells before irradiation, remains the same after exposure to X-rays. The density of replicon clusters simultaneously operating in tandem groups, which is initially much less in XPII cells compared to normal cells, also remains unchanged after exposure to X-rays (5 Gy), since the inhibition of DNA replication occurs to individual replicons only. Our data suggest that the inhibition of DNA replication in normal cells throughout the whole cluster, that drastically reduces the rate of DNA-chain growth, may provide an additional time to restore damaged chromosomes, i. e. it is part of the cellular defence mechanism. It seems likely that XPII cells are deficient in such a defence mechanism.
利用DNA纤维放射自显影技术,对来自正常供体以及对电离辐射敏感的XPII患者的培养成纤维细胞中的DNA复制进行了评估。此处提供的证据表明,XPII细胞在照射前叉移动显著降低,照射X射线后仍保持不变。串联组中同时运行的复制子簇的密度,XPII细胞最初比正常细胞少得多,在暴露于X射线(5 Gy)后也保持不变,因为DNA复制的抑制仅发生在单个复制子上。我们的数据表明,正常细胞中整个簇的DNA复制受到抑制,这极大地降低了DNA链的生长速度,可能为修复受损染色体提供额外的时间,即它是细胞防御机制的一部分。XPII细胞似乎缺乏这种防御机制。