Oxidative stress may contribute to many of the pathophysiologic changes that occur after traumatic brain injury (TBI). There are a number of potential sources and mechanisms for oxygen free radical (OFR) production and lipid peroxiclation after TBI. In this study, we investigate the time-dependent changes in xanthine oxidase (XO) activity and lipid peroxiclation using a focal TBI animal model. We demonstrate that there is an immediate increase in lipid peroxiclation by-products and in XO enzyme activity after TBI. (c) 2005 Elsevier Ltd. All rights reserved.