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First published online August 6, 2004
Journal of Experimental Biology 207, 3221-3231 (2004)
Published by The Company of Biologists 2004
doi: 10.1242/jeb.01022
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Review Article

Oxidants, antioxidants and the ischemic brain

David S. Warner1,3,4,*, Huaxin Sheng1 and Ines Batinic-Haberle2

1 Department of Anesthesiology, The Multidisciplinary Neuroprotection Laboratories, Duke University Medical Center, Durham, NC 27710, USA
2 Department of Radiation Oncology, The Multidisciplinary Neuroprotection Laboratories, Duke University Medical Center, Durham, NC 27710, USA
3 Department of Neurobiology, The Multidisciplinary Neuroprotection Laboratories, Duke University Medical Center, Durham, NC 27710, USA
4 Surgery (Neurosurgery), The Multidisciplinary Neuroprotection Laboratories, Duke University Medical Center, Durham, NC 27710, USA

* Author for correspondence (e-mail: warne002{at}mc.duke.edu)

Accepted 13 April 2004

Despite numerous defenses, the brain is vulnerable to oxidative stress resulting from ischemia/reperfusion. Excitotoxic stimulation of superoxide and nitric oxide production leads to formation of highly reactive products, including peroxynitrite and hydroxyl radical, which are capable of damaging lipids, proteins and DNA. Use of transgenic mutants and selective pharmacological antioxidants has greatly increased understanding of the complex interplay between substrate deprivation and ischemic outcome. Recent evidence that reactive oxygen/nitrogen species play a critical role in initiation of apoptosis, mitochondrial permeability transition and poly(ADP-ribose) polymerase activation provides additional mechanisms for oxidative damage and new targets for post-ischemic therapeutic intervention. Because oxidative stress involves multiple post-ischemic cascades leading to cell death, effective prevention/treatment of ischemic brain injury is likely to require intervention at multiple effect sites.

Key words: brain, ischemia, oxidative stress, antioxidant


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