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Radiation Protection Dosimetry Advance Access published online on December 12, 2006
Radiation Protection Dosimetry, doi:10.1093/rpd/ncl445
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Micros 2005 Special Issue

GENOMIC INSTABILITY AND THE ROLE OF RADIATION QUALITY

M. A. Kadhim 1 *, M. A. Hill 1, and S. R. Moore 1

1 Radiation and Genome Stability Unit, Medical Research Council, Harwell, Oxfordshire, OX11 0RD, UK

* To whom correspondence should be addressed.
M. A. Kadhim, E-mail: m.kadhim{at}har.mrc.ac.uk


  Abstract

Genomic instability (GI) is a hallmark of tumorigenic progression and is observed as delayed genetic damage in the progeny of irradiated and unirradiated bystander cells. The expression of GI can be influenced by genotype, cell type and radiation quality. While several studies have demonstrated the induction of GI by high and low-linear energy transfer (LET) radiation, our work on human and mouse primary cell systems has shown LET-dependent differences in the induction and expression of GI. These differences might be attributed to differences in radiation track structure, dose rate, contribution of bystander cells and radiation dose. This paper reviews the role of radiation quality in the induction of GI and describe the possible mechanisms underlining the observed differences between radiation types on its induction. The experimental results presented suggest that dose might be the most significant factor in determining induction of GI after low-LET radiation.


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