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Biochemistry Research International
Volume 2012, Article ID 896751, 14 pages
Review Article

Mitochondria: Redox Metabolism and Dysfunction

Jia Kang1,2 and Shazib Pervaiz1,2,3,4

1ROS, Apoptosis and Cancer Biology Laboratory, Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597
2NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore 117597
3Cancer and Stem Cell Biology Program, Duke-NUS Graduate Medical School, Singapore 169857
4Cell and Systems Biology (CSB), Singapore-MIT Alliance, Singapore 637460

Received 23 December 2011; Accepted 5 February 2012

Academic Editor: Renée Ventura-Clapier

Copyright © 2012 Jia Kang and Shazib Pervaiz. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mitochondria are the main intracellular location for fuel generation; however, they are not just power plants but involved in a range of other intracellular functions including regulation of redox homeostasis and cell fate. Dysfunction of mitochondria will result in oxidative stress which is one of the underlying causal factors for a variety of diseases including neurodegenerative diseases, diabetes, cardiovascular diseases, and cancer. In this paper, generation of reactive oxygen/nitrogen species (ROS/RNS) in the mitochondria, redox regulatory roles of certain mitochondrial proteins, and the impact on cell fate will be discussed. The current state of our understanding in mitochondrial dysfunction in pathological states and how we could target them for therapeutic purpose will also be briefly reviewed.