Review ArticleFree Radicals, Antioxidants, and Neurologic Injury: Possible Relationship to Cerebral Protection by AnestheticsWilson, John X.; Gelb, Adrian W.Author Information Departments of Physiology and Anaesthesia, University of Western Ontario, London, Ontario, Canada Address correspondence and reprint requests to Dr. Adrian W. Gelb, Department of Anesthesia, London Health Sciences Center, 339 Windermere Rd., London, Canada NGA 5A5. Accepted for publication June 26, 2001. Journal of Neurosurgical Anesthesiology: January 2002 - Volume 14 - Issue 1 - p 66-79 Buy Abstract Oxygen-centered free radicals cause brain injury associated with trauma and stroke. These reactive oxygen species may be detoxified by endogenous antioxidants, but cell death occurs after antioxidants become depleted. General anesthetics penetrate into brain parenchyma, where they may abrogate oxidative injury to neurons by several mechanisms that prevent the initiation of free radical chain reactions or terminate the propagation of highly reactive radicals. First, general anesthetics may inhibit free radical generation because these drugs slow cerebral utilization of oxygen and glucose, inhibit oxidative metabolism in neutrophils, and prevent redox changes in hemoglobin. Second, antioxidant anesthetics, such as thiopental and propofol, directly scavenge reactive oxygen species and inhibit lipid peroxidation. Finally, anesthetics may prevent the elevation of extracellular glutamate concentration and inhibit the activation of excitatory glutamatergic receptors that augment oxidative stress after ischemia. © 2002 Lippincott Williams & Wilkins, Inc.