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Neurology Research International
Volume 2012, Article ID 542976, 10 pages
Review Article

Hypoxic-Ischemic Injury in the Developing Brain: The Role of Reactive Oxygen Species Originating in Mitochondria

1Department of Pediatrics, Columbia University, NY, USA
2Department of Neurology and Neuroscience, Cornell University, NY, USA
3Division of Neonatology, Department of Pediatrics, Morgan Stanley Children’s Hospital of New York, 3959 Broadway, BHN 1201, New York, NY 10032, USA

Received 6 September 2011; Revised 12 November 2011; Accepted 22 November 2011

Academic Editor: Robin L. Haynes

Copyright © 2012 Vadim S. Ten and Anatoly Starkov. 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.


Mitochondrial dysfunction is the most fundamental mechanism of cell damage in cerebral hypoxia-ischemia and reperfusion. Mitochondrial respiratory chain (MRC) is increasingly recognized as a source for reactive oxygen species (ROS) in the postischemic tissue. Potentially, ROS originating in MRC can contribute to the reperfusion-driven oxidative stress, promoting mitochondrial membrane permeabilization. The loss of mitochondrial membranes integrity during reperfusion is considered as the major mechanism of secondary energy failure. This paper focuses on current data that support a pathogenic role of ROS originating from mitochondrial respiratory chain in the promotion of secondary energy failure and proposes potential therapeutic strategy against reperfusion-driven oxidative stress following hypoxia-ischemia-reperfusion injury of the developing brain.