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Papers Presented at the 2nd Workshop on Radiation and Multidrug Resistance Mediated via the Tumour-Microenvironment

DNA double-strand break signalling: X-ray energy dependence of residual co-localised foci of γ-H2AX and 53BP1

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Pages 1042-1050 | Received 09 Apr 2009, Accepted 16 Jul 2009, Published online: 06 Nov 2009
 

Abstract

Purpose: The application of ionising radiation for medical purposes requires the investigation of induced and persistent DNA damages, especially for soft X-rays that are assumed to be more effective than higher energy photons. Therefore, we examined the energy dependent time and dose response of residual DNA damage foci for soft X-rays in comparison to 200 kV photons.

Materials and methods: DNA damage present in cell line 184A1 within 48 h after irradiations with 10 kV, 25 kV and 200 kV photons was analysed by immunochemical detection of co-localised γ-H2AX (phosphorylated histone H2AX) and 53BP1 (tumour protein 53 binding protein) foci.

Results: The dose dependencies of the colocated foci revealed significant energy dependent differences with increasing amounts of residual foci at decreasing X-ray energy independent on postirradiation time. Dose-dependent RBE (relative biological effectiveness) values ranging from 4 to 7 were determined for 10 kV relative to 200 kV X-rays based on the 24 hour dose responses. For 25 kV photons, ratios considerably higher than one were obtained only for doses above 2 Gy.

Conclusions: The expected energy dependence with increasing DNA damage at decreasing photon energy was confirmed for the residual co-localised foci measured at different time points after irradiation.

Acknowledgements

The authors are grateful to Dr N. Cordes for providing protocols and fruitful discussions, K. Storch for her introduction to the work, and F. Leonhard for her assistance during the experiments. We also thank Dr L. Karsch for the performance of the GEANT4 simulations. The work was supported by the BMBF, Grant No. 03ZIK042.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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