spacer gif spacer gif spacer gif spacer gif spacer gif
QUICK SEARCH:   [advanced]


spacer gif
     Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents    

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
This Article
Right arrow Summary Freely available
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Related articles in JEB
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Warner, D. S.
Right arrow Articles by Batinic-Haberle, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Warner, D. S.
Right arrow Articles by Batinic-Haberle, I.

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



View larger version (14K):

[in a new window]
  		Fig. 1. Ischemia/reperfusion presents numerous opportunities for formation of reactive oxygen/nitrogen species and resultant tissue injury. Simultaneously, numerous site-specific targets for therapeutic intervention are presented. It quickly becomes clear that inhibition of a single pathway may be insufficient to provide persistent protection against oxidative stress. (1) Inhibition of lipid peroxidation; (2) inhibition of xanthine oxidase; (3) the superoxide dismutases (SOD) and their mimetics; (4) catalase and glutathione peroxidase (GSHPx); (5) glutathione (GSH) mimetics; (6) nitric oxide synthase (NOS) inhibition; (7) metal chelators; (8) poly(ADP-ribose) polymerase (PARP) inhibitors; (9) mitochondrial permeability transition inhibitors; (10) spin traps and peroxynitrite scavengers. O2·–, superoxide; CO3·–, carbonate radical; H2O2, hydrogen peroxide; GSSG, glutathione disulfide; ·OH, hydroxyl radical; ·NO2, nitrogen dioxide; ·NO, nitric oxide; ONOO– nicotinamide adenine dinucleotide. peroxynitrite; NAD,

 




© The Company of Biologists Ltd 2004