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中国仓鼠卵巢细胞系X射线敏感突变体(xrs)中的辐射诱导染色体损伤。

Radiation-induced chromosome damage in X-ray-sensitive mutants (xrs) of the Chinese hamster ovary cell line.

作者信息

Kemp L M, Jeggo P A

出版信息

Mutat Res. 1986 Nov;166(3):255-63. doi: 10.1016/0167-8817(86)90025-8.

DOI:10.1016/0167-8817(86)90025-8
PMID:3785270
Abstract

The frequency of both spontaneous and X-ray- (95 rad) induced cytogenetical aberrations has been determined for 2 X-ray-sensitive strains (xrs-6 and xrs-7) of the Chinese hamster ovary cell line, and their wild-type parent (CHO-K1). Increased levels of spontaneous aberrations were not a general feature of the xrs strains, although xrs-7 did show a 2-fold increase in chromatid gaps. Unsynchronied populations of xrs cells, estimated to have been irradiated in late S and G2, showed a 3-5-fold increase in chromatid gaps, breaks and exchanges compared to CHO-K1. The irradiation of synchronised populations of xrs-7 and CHO-K1 in G1 demonstrated a 3-5-fold increase in chromosome breaks, gaps and exchanges in xrs-7. In addition xrs-7 displayed a large increase in chromatid-type aberrations, particularly triradials. These X-ray-sensitive strains have previously been shown to have a defect in double-strand break rejoining (Kemp et al., 1984), and an increased number of double-strand breaks (DBSs) remain in their DNA after irradiation compared to wild-type cells. The increased number of DSBs remaining in these strains 20 min after irradiation, correlates well with the increase in chromosome breaks.

摘要

已测定了中国仓鼠卵巢细胞系的2个X射线敏感株(xrs - 6和xrs - 7)及其野生型亲本(CHO - K1)的自发和X射线(95拉德)诱导的细胞遗传学畸变频率。自发畸变水平升高并非xrs株的普遍特征,尽管xrs - 7的染色单体间隙确实增加了2倍。估计在S期晚期和G2期受到照射的未同步化xrs细胞群体,与CHO - K1相比,染色单体间隙、断裂和交换增加了3至5倍。对处于G1期的xrs - 7和CHO - K1同步化群体进行照射,结果显示xrs - 7的染色体断裂、间隙和交换增加了3至5倍。此外,xrs - 7的染色单体型畸变大幅增加,尤其是三辐射体。这些X射线敏感株此前已被证明在双链断裂重新连接方面存在缺陷(肯普等人,1984年),与野生型细胞相比,照射后其DNA中残留的双链断裂(DSB)数量增加。照射后20分钟这些株系中残留的DSB数量增加,与染色体断裂的增加密切相关。

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Radiation-induced chromosome damage in X-ray-sensitive mutants (xrs) of the Chinese hamster ovary cell line.中国仓鼠卵巢细胞系X射线敏感突变体(xrs)中的辐射诱导染色体损伤。
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