Recently there has been considerable interest in various delayed effects of radiation. These have the common property of showing a high and, in some instances, non-clonal transmission of 'damage' to distant progeny which derive from apparently normal surviving cells and their descendants. This means that conventional analysis and interpretation of long-term radiation damage in terms of mutations induced in DNA at the time of radiation exposure may be incorrect. Several reviews of this area have appeared in recent years which have described the historical development of this field. The aim of this commentary is to highlight areas of discussion, particularly concerning links between the various end-points, and to discuss some of the possible implications of genomic instability for radiation carcinogenesis in general and for the setting of radiation protection action limits in particular.
CITATION STYLE
Mothersill, C., & Seymour, C. B. (1998). Mechanisms and implications of genomic instability and other delayed effects of ionizing radiation exposure. Mutagenesis. https://doi.org/10.1093/mutage/13.5.421
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