Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 21, Issue 1, Pages 2-14Publisher
SAGE PUBLICATIONS INC
DOI: 10.1097/00004647-200101000-00002
Keywords
reactive oxygen species; free radicals; apoptosis; cerebral ischemia; transgenic and knockout mice; oxidative stress signaling
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Funding
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P50NS014543, R01NS036147, P01NS014543, R01NS025372] Funding Source: NIH RePORTER
- NINDS NIH HHS [NS25372, NS14543, NS36147] Funding Source: Medline
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Reactive oxygen species have been implicated in brain injury after ischemic stroke. These oxidants can react and damage the cellular macromolecules by virtue of the reactivity that leads to cell injury and necrosis. Oxidants an also media- tors in signaling involving mitnchondria, DNA repair enzymes, and transcription factors that may lead to apoptosis after cerebral ischemia. Transgenic or knockout mice with cell- or site-specific prooxidant and antioxidant enzymes provide useful tools in dissecting the events involving oxidative stress in signaling and damage in ischemic brain injury.
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