Interdisciplinary Bio Central
Review (Biological frontiers (General Biology))

Mitochondrial DNA Mutation and Oxidative Stress
Taeho Kim1+, Hans H. Kim2+ and Hyun Joo3,*
1Biological Resources Coordination Division, National Institute of Biological Resources, Incheon 404-708, Republic of Korea
2College of Medicine, SUNY Upstate Medical University, Syracuse, New York 13210, USA
3Department of Physiology and Integrated Biosystems, School of Medicine, Inje University, Busan 614-735, Republic of Korea
*Corresponding author
+These authors contributed equally to this work
  Received : December 29, 2011
  Accepted : December 30, 2011
  Published : December 30, 2011
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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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.

Keyword: mitochondrial disease, reactive oxygen species (ROS), mitochondrial apoptosis, mitochondrial DNA mutation, mitochondrial permeability transition pore
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