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Mutagenesis Advance Access published online on October 25, 2006
Mutagenesis, doi:10.1093/mutage/gel048
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© The Author 2006. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received August 26, 2006
Revised September 7, 2006
Accepted September 15, 2006

Review

Mitochondrial dysfunction, persistently elevated levels of reactive oxygen species and radiation-induced genomic instability: a review

Grace J. Kim 1 *, Krish Chandrasekaran 2, and William F. Morgan 3

1 Graduate Program in Molecular and Cell Biology, University of Maryland, Baltimore, 108 North Greene Street, BRF Room 110C, Baltimore, MD 21201, USA; Radiation Oncology Research Laboratory, University of Maryland School of Medicine, 685 West, Baltimore Street, MSTF 5-34, Baltimore, MD 21201, USA
2 Department of Anesthesiology, University of Maryland School of Medicine, 685 West, Baltimore Street, MSTF 5-34, Baltimore, MD 21201, USA
3 Radiation Oncology Research Laboratory, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201, USA; Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201, USA

* To whom correspondence should be addressed.
Grace J. Kim, E-mail: gkim002{at}umaryland.edu


  Abstract

Radiation-induced genomic instability (RIGI) challenges the long-standing notion that radiation's effects derive solely from nuclear impact. In RIGI it is the unirradiated progeny that can display phenotypic changes at delayed times after irradiation of the parental cell. RIGI might well provide the driving force behind the development of radiation-induced tumorigenesis as most cancer cells even in pre-neoplastic states display multiple genetic alterations. Thus, understanding RIGI may help elucidate the mechanisms underlying radiation-induced carcinogenesis. One characteristic of clones of genetically unstable cells is that many exhibit persistently increased levels of reactive oxygen species (ROS). Furthermore, oxidants enhance and antioxidants diminish radiation-induced instability. However, much about the mechanisms behind the initiation and perpetuation of RIGI remains unknown and we examine the evidence for the hypothesis that oxidative stress and mitochondrial dysfunction may be involved in perpetuating the unstable phenotype in some cell clones surviving ionizing radiation.


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