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DNA damage interactions on both nanometer and micrometer scale determine overall cellular damage.
Sci. Rep. 8:16063 (2018)
Verlagsversion
Forschungsdaten
DOI
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,
Artikelnummer: 16063
Verlag
Nature Publishing Group
Verlagsort
London
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Radiation Medicine (IRM)