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Radiation-induced genomic instabilityQuantitative assessment of the heritable somatic effects of ionizing radiation exposures has relied upon the assumption that radiation-induced lesions were 'fixed' in the DNA prior to the first postirradiation mitosis. Lesion conversion was thought to occur during the initial round of DNA replication or as a consequence of error-prone enzymatic processing of lesions. The standard experimental protocols for the assessment of a variety of radiation-induced endpoints (cell death, specific locus mutations, neoplastic transformation and chromosome aberrations) evaluate these various endpoints at a single snapshot in time. In contrast with the aforementioned approaches, some studies have specifically assessed radiation effects as a function of time following exposure. Evidence has accumulated in support of the hypothesis that radiation exposure induces a persistent destabilization of the genome. This instability has been observed as a delayed expression of lethal mutations, as an enhanced rate of accumulation of non-lethal heritable alterations, and as a progressive intraclonal chromosomal heterogeneity. The genetic controls and biochemical mechanisms underlying radiation-induced genomic instability have not yet been delineated. The aim is to integrate the accumulated evidence that suggests that radiation exposure has a persistent effect on the stability of the mammalian genome.
Document ID
Document Type
Reprint (Version printed in journal)
Kronenberg, A.
(Lawrence Berkeley Laboratory Berkeley, CA 94720)
Date Acquired
August 22, 2013
Publication Date
November 1, 1994
Publication Information
Publication: International journal of radiation biology
Volume: 66
Issue: 5
ISSN: 0955-3002
Subject Category
Life Sciences (General)
Distribution Limits
NASA Discipline Radiation Health
Non-NASA Center

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