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Impact of dimethyl sulfoxide on irradiation-related DNA double-strand-break induction, -repair and cell survival.
Radiation and Environmental Biophysics ( IF 1.7 ) Pub Date : 2019-05-28 , DOI: 10.1007/s00411-019-00797-y
Felix Zwicker 1, 2 , Henrik Hauswald 2 , Jürgen Debus 1, 2 , Peter E Huber 1, 2 , Klaus-Josef Weber 2
Affiliation  

Dimethyl sulfoxide (DMSO) is an effective radical scavenger and, when added to cells, reduces the initial number of radiation-induced DNA double-strand breaks (DSB). The aim of this study was to investigate modification by DMSO of both DSB induction and DSB repair by means of pulsed-field gel electrophoresis (PFGE) as well as gamma-H2AX immunofluorescence staining. WiDr cells (human colon carcinoma provided by DKFZ) were incubated with 2% DMSO for 2 h (or mock-treated) prior to irradiation with varying X-ray doses and subsequent incubation for repair. Sample processing for PFGE analysis or counting of γ-H2AX foci was performed according to standard protocols. Effects on apoptosis induction and cell survival were investigated additionally by standard protocols. DMSO reduced DSB yield after 20-80 Gy measured by PFGE. A qualitatively similar result was found after low-dose irradiation (1 Gy) using γ-H2AX immunofluorescence staining. During incubation for repair, both DNA fragment rejoining (PFGE) as well as γ-H2AX foci removal occurred at a reduced rate when cells had been pre-treated with DMSO. But this effect was clearly more pronounced for the PFGE-analyzed double-strand breakage, particularly at early repair times. WiDr cells treated with DMSO (2%) showed a significantly increased clonogenic survival after irradiation doses above 8 Gy. Apoptosis rates were not changed by DMSO. The radio-protective effect of DMSO, well known from other PFGE studies, could be confirmed for the formation of γ-H2AX foci. DSB generated in the presence of DMSO were less rapidly repaired. DMSO showed radio-protective effects on clonogenic survival but not on apoptosis.

中文翻译:

二甲基亚砜对辐射相关DNA双链断裂诱导,修复和细胞存活的影响。

二甲基亚砜(DMSO)是一种有效的自由基清除剂,当添加到细胞中时,可减少辐射诱导的DNA双链断裂(DSB)的初始数目。这项研究的目的是通过脉冲场凝胶电泳(PFGE)以及γ-H2AX免疫荧光染色研究DMSO对DSB诱导和DSB修复的修饰。将WiDr细胞(由DKFZ提供的人结肠癌)与2%DMS​​O孵育2小时(或模拟处理),然后用不同的X射线剂量照射并随后孵育以进行修复。根据标准方案进行PFGE分析或γ-H2AX病灶计数的样品处理。通过标准方案另外研究了对凋亡诱导和细胞存活的影响。通过PFGE测量,DMSO在20-80 Gy后降低了DSB产量。使用γ-H2AX免疫荧光染色在低剂量照射(1 Gy)后发现了定性相似的结果。在进行修复的温育过程中,当细胞已用DMSO预处理时,DNA片段重新连接(PFGE)以及γ-H2AX病灶的去除均以降低的速率发生。但是,对于PFGE分析的双链断裂,这种影响显然更为明显,尤其是在早期维修时。用DMSO(2%)处理的WiDr细胞在照射剂量超过8 Gy后显示出明显的克隆形成存活。DMSO未改变细胞凋亡率。其他PFGE研究众所周知,DMSO的辐射防护作用可用于形成γ-H2AX灶。在DMSO存在下生成的DSB修复速度较慢。DMSO显示出对克隆形成存活的辐射防护作用,但对细胞凋亡没有作用。
更新日期:2019-11-01
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