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Mitochondrial DNA Mutation and Oxidative Stress

  • Kim, Tae-Ho (Biological Resources Coordination Division, National Institute of Biological Resources) ;
  • Kim, Hans-H. (College of Medicine, SUNY Upstate Medical University) ;
  • Joo, Hyun (Department of Physiology and Integrated Biosystems, School of Medicine, Inje University)
  • Received : 2011.12.28
  • Accepted : 2011.12.30
  • Published : 2011.12.30

Abstract

Defects in mitochondrial DNA (mtDNA) cause many human diseases and are critical factors that contribute to aging. The mechanisms of maternally-inherited mtDNA mutations are well studied. However, the role of acquired mutations during the aging process is still poorly understood. The most plausible mechanism is that increased reactive oxygen species (ROS) may affect the opening of mitochondrial voltage dependent anion channel (VDAC) and thus results in damage to mtDNA. This review focuses on recent trends in mtDNA research and the mutations that appear to be associated with increased ROS.

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