University of Sussex
Browse

File(s) not publicly available

The role of the DNA damage response mechanisms after low-dose radiation exposure and a consideration of potentially sensitive individuals

journal contribution
posted on 2023-06-07, 15:32 authored by Penny Jeggo
Here I consider whether radiation-sensitive individuals might exist in the population and the potential impact of low-dose/dose-rate radiation exposure. Radiation induces DNA double-strand breaks (DSBs), which cause lethality if they are unrepaired and enhance genomic instability if they are misrepaired. DNA damage response (DDR) mechanisms play a vital role in protecting cells from the harmful effects of DSB formation. The DDR encompasses DSB repair pathways, of which DNA nonhomologous end joining is the most significant, and a signal transduction process involving ATM. Patients defective in DDR proteins have been described, and some have shown clinical radiosensitivity. However, such patients are rare and belong to defined syndromes. The critical question is whether heterozygosity or mild defects in DDR proteins confer low-dose radiosensitivity. While it is unlikely that low-dose radiation will dramatically enhance cell killing in such patients, it is possible that there could be an impact on stem cell turnover, leading to stem cell depletion with age. More importantly, it is likely that such patients could have increased misrepair of radiation damage and hence an elevated risk of radiation-induced carcinogenesis. Evidence in support of this and the potentially important genes in this context are discussed

History

Publication status

  • Published

Journal

Radiation Research

ISSN

0033-7587

Publisher

Radiation Research Society

Issue

6b

Volume

174

Page range

825-832

Department affiliated with

  • Sussex Centre for Genome Damage Stability Publications

Notes

GDSC315

Full text available

  • No

Peer reviewed?

  • Yes

Legacy Posted Date

2010-08-19

Usage metrics

    University of Sussex (Publications)

    Categories

    No categories selected

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC