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DNA damage interactions on both nanometer and micrometer scale determine overall cellular damage.
Sci. Rep. 8:16063 (2018)
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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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
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
Journal
Scientific Reports
Quellenangaben
Volume: 8,
Issue: 1,
Article Number: 16063
Publisher
Nature Publishing Group
Publishing Place
London
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Radiation Medicine (IRM)