Abstract
Protontherapy has emerged as more effective in the treatment of certain tumors than photon based therapies. However, significant capital and operational costs make protontherapy less accessible. This has stimulated interest in alternative proton delivery approaches, and in this context the use of laser-based technologies for the generation of ultra-high dose rate ion beams has been proposed as a prospective route. A better understanding of the radiobiological effects at ultra-high dose-rates is important for any future clinical adoption of this technology. In this study, we irradiated human skin fibroblasts-AG01522B cells with laser-accelerated protons at a dose rate of 109 Gy/s, generated using the Gemini laser system at the Rutherford Appleton Laboratory, UK. We studied DNA double strand break (DSB) repair kinetics using the p53 binding protein-1(53BP1) foci formation assay and observed a close similarity in the 53BP1 foci repair kinetics in the cells irradiated with 225 kVp X-rays and ultra- high dose rate protons for the initial time points. At the microdosimetric scale, foci per cell per track values showed a good correlation between the laser and cyclotron-accelerated protons indicating similarity in the DNA DSB induction and repair, independent of the time duration over which the dose was delivered.
Highlights
Rate of the order of 109 Gy per second, many orders of magnitude higher than that of conventional ion beams
Three publications have so far reported Gy-level irradiation in single pulses, at ultra-high dose rates[8,9,15], which is the approach used here to study the DNA double strand break (DSB) damage and repair kinetics induced by single pulses of laser-accelerated 10 MeV protons at an ultra-high dose rate of 109 Gy/s
DNA DSB damage repair kinetics induced by laser-accelerated protons
Summary
Rate of the order of 109 Gy per second, many orders of magnitude higher than that of conventional ion beams (typically Gy/min) Under these conditions, effects related to the ultrashort dose deposition have been suggested as possible causes for variations in the biological response of the irradiated cell, namely through possible alteration of the indirect DNA damage associated to free radical production (oxygen depletion effect)[14] or, at sufficiently high doses, spatio-temporal overlap of independent tracks resulting in collective effects[15]. We used a well-referenced radiobiologically relevant human cell line AG01522B17–19 and compared our results with lower LET X-rays and cyclotron accelerated protons
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