Reactive oxygen radicals in signaling and damage in the ischemic brain.
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 are also mediators in signaling involving mitochondria, 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.
Chan
P H
PH
Department of Neurosurgery, Stanford University School of Medicine, California 94205-5487, USA.
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001921:Brain / Q000503:physiopathology*; D002545:Brain Ischemia / Q000503:physiopathology*; D006801:Humans; D008959:Models, Neurological; D016877:Oxidants / Q000378:metabolism; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000502:physiology*; D015398:Signal Transduction
D000975:Antioxidants; D016877:Oxidants; D017382:Reactive Oxygen Species