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2-氯脱氧腺苷抑制X射线照射的中国仓鼠V79细胞中DNA双链断裂的修复,但不抑制DNA单链断裂的修复。

2-Chlorodeoxyadenosine inhibits the repair of DNA double-strand breaks and does not inhibit the repair of DNA single-strand breaks in X-irradiated Chinese hamster V79 cells.

作者信息

Kuwabara M, Tanabe K, Hiraoka W, Tamura Y, Sato F, Matsuda A, Ueda T

机构信息

Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan.

出版信息

Chem Biol Interact. 1991;79(3):349-58. doi: 10.1016/0009-2797(91)90114-m.

Abstract

The exposure of log-phase Chinese hamster V79 cells to 2-chlorodeoxyadenosine (CdA) for 3 h after X irradiation enhanced the lethal effects of X-rays in a concentration-dependent manner. The enhancement of the killing efficiency of X-rays by CdA was mainly observed in the reduction of quasi-threshold doses (Dq) of the dose-response curves. When the ability of CdA to inhibit the repair of X-ray-induced double- and single-strand breaks (dsb and ssb) of DNA was investigated by neutral- and alkaline-filter elution techniques, respectively, it was observed that 90% of dsb were rejoined in the absence of CdA within 30 min after X irradiation and 15-40% of dsb rejoining was suppressed by co-incubation of the cells with 5-10 microM of CdA for 3 h after X irradiation, whereas almost 100% of ssb were rejoined within 15 min regardless of the presence or absence of CdA. From these results it was concluded that CdA interfered exclusively with the repair of DNA dsb in X-irradiated Chinese hamster V79 cells and thereby increased the lethality of X-rays.

摘要

对数期中国仓鼠V79细胞在X射线照射后用2-氯脱氧腺苷(CdA)处理3小时,可呈浓度依赖性增强X射线的致死效应。CdA对X射线杀伤效率的增强主要表现为剂量反应曲线的准阈值剂量(Dq)降低。当分别用中性和碱性滤膜洗脱技术研究CdA抑制X射线诱导的DNA双链和单链断裂(dsb和ssb)修复的能力时,观察到在X射线照射后30分钟内,90%的dsb在无CdA的情况下重新连接,而在X射线照射后用5-10 microM的CdA与细胞共同孵育3小时,可抑制15-40%的dsb重新连接,而无论有无CdA,几乎100%的ssb在15分钟内重新连接。从这些结果得出结论,CdA仅干扰X射线照射的中国仓鼠V79细胞中DNA dsb的修复,从而增加了X射线的致死性。

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