Free Radical Production

Abstract

Among the pathomechanisms involved with traumatic brain and spinal cord injury, reactive oxygen species and lipid peroxidation play an important role [3,4]. In a model of global cerebral ischemia, Baiping and colleagues [1] reported that moderate hypothermia (30°–32°C) attenuated lipid peroxidation. In a model of fluid-percussion brain injury, posttraumatic hypothermia (30°C) reduced the production of free radicals, as measured by the hydroxylation of salicylate by hydroxyl radicals to produce 2,5-dihydroxybenzoic acid, compared with normothermic trauma [2]. Interestingly, a significant correlation between the magnitude of glutamate release and the extent of hydroxyl radical production was demonstrated in that study, suggesting a link between the two responses. Posttraumatic hypothermia may therefore improve outcome by attenuating free radical formation and excitotoxicity. A current question is whether these relatively early posttraumatic events can be successfully targeted for treatment.