首页> 外文期刊>International Journal of Radiation Biology: Covering the Physical, Chemical, Biological, and Medical Effects of Ionizing and Non-ionizing Radiations >Induction of chromosome aberrations in unirradiated chromatin after partial irradiation of a cell nucleus.
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Induction of chromosome aberrations in unirradiated chromatin after partial irradiation of a cell nucleus.

机译:细胞核部分辐照后未辐照的染色质中染色体畸变的诱导。

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PURPOSE: It is generally accepted that chromosome exchanges in irradiated cells are formed through interactions between separate DNA double-strand breaks (DSB). Here we tested whether non-irradiated DNA participates in the formation of chromosome aberrations when complex DNA DSB are induced elsewhere in the nucleus. MATERIALS AND METHODS: Synchronized Chinese hamster cells containing an X chromosome with a late replicating q arm (X(q) domain) were labelled with 125I-iododeoxyuridine (125IdUrd) in a period of S-phase when the vast majority of the X(q) domain was not replicating. DNA damage from 125I decay was accumulated at the G1/S border while the cells were stored in liquid nitrogen. Decay of 125I induced DSB in the immediate vicinity of the 125I atom. Chromosome aberrations involving what is essentially the 125I-free X domain were scored at the first mitosis after cell thawing. As a positive control, cells were treated with 125IdUrd at a later period in S-phase when the X(q) domain replicates, yielding a labelled X(q) domain. RESULTS: The 125I-free X(q) domain exhibited chromosome aberrations (exchanges and fragments). The frequency of these aberrations was linearly dependent on the number of 125I decays elsewhere in the cell nucleus. The efficiency of formation of chromosome aberrations by the 125I-free X(q) domain was approximately half of that observed in the 125I-labelled X(q) domain. CONCLUSIONS: The involvement of the 125I-free X(q) domain in chromosome aberrations suggests that DNA not damaged by the decay of incorporated 125I can interact with damaged DNA, indicating the existence of an alternative pathway for the formation of chromosome aberrations.
机译:目的:通常认为,受辐照细胞中的染色体交换是通过单独的DNA双链断裂(DSB)之间的相互作用形成的。在这里,我们测试了当在核中其他位置诱导复杂的DNA DSB时,未辐照的DNA是否参与染色体畸变的形成。材料与方法:当绝大多数X(q)处于X期时,在S期以125I-碘脱氧尿苷(125IdUrd)标记含有X染色体且复制后的q臂(X(q)域)的同步中国仓鼠细胞。 )域未复制。 125I衰变引起的DNA损伤累积在G1 / S边界,而细胞则存储在液氮中。 125I的衰变在紧邻125I原子的位置诱导了DSB。在融化后的第一个有丝分裂中,对涉及本质上是无125 I的X结构域的染色体畸变进行评分。作为阳性对照,当X(q)域复制时,在S期的后期用125IdUrd处理细胞,产生标记的X(q)域。结果:无125 I的X(q)域表现出染色体畸变(交换和碎片)。这些像差的频率线性依赖于细胞核其他部位125 I衰变的数量。由无125 I的X(q)域形成染色体畸变的效率大约是在125I标记的X(q)域中观察到的效率的一半。结论:染色体畸变中无125 I的X(q)结构域的参与表明未受掺入的125 I破坏的DNA可以与受损的DNA相互作用,表明存在形成染色体畸变的替代途径。

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