Impact of dimethyl sulfoxide on irradiation-related DNA double-strand-break induction, -repair and cell survival

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 electr...

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Hauptverfasser: Zwicker, Felix (VerfasserIn) , Hauswald, Henrik (VerfasserIn) , Debus, Jürgen (VerfasserIn) , Huber, Peter E. (VerfasserIn) , Weber, Klaus-Josef (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 2019
In: Radiation and environmental biophysics
Year: 2019, Jahrgang: 58, Heft: 3, Pages: 417-424
ISSN:1432-2099
DOI:10.1007/s00411-019-00797-y
Online-Zugang:Verlag, Volltext: https://doi.org/10.1007/s00411-019-00797-y
Volltext
Verfasserangaben:Felix Zwicker, Henrik Hauswald, Jürgen Debus, Peter E. Huber, Klaus-Josef Weber

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520 |a 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. 
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