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Friedrich, T.* ; Ilicic, K. ; Greubel, C.* ; Girst, S.* ; Reindl, J.* ; Sammer, M.* ; Schwarz, B.* ; Siebenwirth, C.* ; Walsh, D.W.M.* ; Schmid, T.E. ; Scholz, M.* ; Dollinger, G.*

DNA damage interactions on both nanometer and micrometer scale determine overall cellular damage.

Sci. Rep. 8:16063 (2018)
Verlagsversion Forschungsdaten DOI
Open Access Gold
Creative Commons Lizenzvertrag
DNA double strand breaks (DSB) play a pivotal role for cellular damage, which is a hazard encountered in toxicology and radiation protection, but also exploited e.g. in eradicating tumors in radiation therapy. It is still debated whether and in how far clustering of such DNA lesions leads to an enhanced severity of induced damage. Here we investigate - using focused spots of ionizing radiation as damaging agent - the spatial extension of DNA lesion patterns causing cell inactivation. We find that clustering of DNA damage on both the nm and pm scale leads to enhanced inactivation compared to more homogeneous lesion distributions. A biophysical model interprets these observations in terms of enhanced DSB production and DSB interaction, respectively. We decompose the overall effects quantitatively into contributions from these lesion formation processes, concluding that both processes coexist and need to be considered for determining the resulting damage on the cellular level.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Double-strand Breaks; Lethal Radiation-damage; Repair Pathway Choice; 20 Mev Protons; Track-structure; Human-cells; Irradiation; Chromatin; Complexity; Survival
ISSN (print) / ISBN 2045-2322
e-ISSN 2045-2322
Zeitschrift Scientific Reports
Quellenangaben Band: 8, Heft: 1, Seiten: , Artikelnummer: 16063 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed