A MODEL RELATING CELL-SURVIVAL TO DNA FRAGMENT LOSS AND UNREPAIRED DOUBLE-STRAND BREAKS
A MODEL RELATING CELL-SURVIVAL TO DNA FRAGMENT LOSS AND UNREPAIRED DOUBLE-STRAND BREAKS
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DOI：
10.2307/3577405
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发表时间：
1989-06-01
影响因子：
3.4
通讯作者：
OSTASHEVSKY, JY
中科院分区：
文献类型：
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作者：
OSTASHEVSKY, JY
所提出的辐射作用模型将受辐射细胞的存活率与未修复的DNA双链断裂(DSB)联系起来。该模型假设：(I)由诱导的DSB产生的DNA片段可能移出其染色体(丢失)，这一过程的概率取决于片段的大小；(Ii)如果受照射的细胞在细胞周期的特定时间点有未修复的DSB(包括DNA片段)，则它将失去其增殖能力。该模型的数学表达式给出了存活部分的剂量和时间依赖关系、未修复的DSB的数量以及永久凝聚的染色体片段的数量。所描述的放射生物学现象包括低剂量率、延迟电镀、高渗溶液、ARAA和高LET辐射的影响。共济失调毛细血管扩张症和正常成纤维细胞的未修复DSB剩余数量的计算剂量依赖关系与实验获得的非常接近[M.N.Cornforts和J.S.Bedford，Radiat。第111,385-405号决议(1987)]染色体异常总数。这导致了这样的结论：每一个未修复的DSB都会变成染色体的异常。根据模型的分析表明，不同细胞系的辐射敏感性主要是由于这些细胞中可用于DSB修复的时间不同所致。
The model of radiation action that is presented relates the surviving fraction of irradiated cells to unrepaired DNA double-strand breaks (DSBs). The following assumptions are made in the model: (i) A DNA fragment created by the induced DSBs may move out of its chromosome (become lost), and the probability of that process depends on the fragment size, (ii) An irradiated cell will lose its proliferative capacity if it has an unrepaired DSB (including DNA fragments) at certain points in the cell cycle. Mathematical expressions of the model yield the dose and time dependencies of the surviving fraction, the number of unrepaired DSBs, and the number of permaturely condensed chromosome fragments. Radiobiological phenomena described include effects of low dose rate, delayed plating, hypertonic solution, araA, and high-LET radiation. The calculated dose dependence of the residual number of unrepaired DSBs for ataxia telangiectasia and normal fibroblasts cells is very close to the experimentally obtained [M. N. Cornforth and J. S. Bedford, Radiat. Res 111, 385-405 (1987)] total number of chromosomal aberrations. This leads to the conclusion that each unrepaired DSB becomes a chromosomal aberration. Analysis in terms of the model shows that the radiosensitivity of various cell lines is predominantly due to the different amounts of time available for DSB repair in these cells.