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

Published

Journal Article (Review)

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.

Full Text

Duke Authors

Cited Authors

  • Kim, GJ; Chandrasekaran, K; Morgan, WF

Published Date

  • November 2006

Published In

Volume / Issue

  • 21 / 6

Start / End Page

  • 361 - 367

PubMed ID

  • 17065161

Pubmed Central ID

  • 17065161

International Standard Serial Number (ISSN)

  • 0267-8357

Digital Object Identifier (DOI)

  • 10.1093/mutage/gel048

Language

  • eng

Conference Location

  • England