Increased xanthine oxidase activity after traumatic brain injury in rats

J Clin Neurosci. 2005 Apr;12(3):273-5. doi: 10.1016/j.jocn.2004.12.002.


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 peroxidation after TBI. In this study, we investigate the time-dependent changes in xanthine oxidase (XO) activity and lipid peroxidation using a focal TBI animal model. We demonstrate that there is an immediate increase in lipid peroxidation by-products and in XO enzyme activity after TBI.

MeSH terms

  • Animals
  • Brain / enzymology
  • Brain Injuries / enzymology*
  • Brain Injuries / pathology
  • Cytoplasm / enzymology
  • Free Radicals / metabolism
  • Lipid Peroxidation / drug effects
  • Male
  • Nitric Oxide Synthase / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Thiobarbituric Acid Reactive Substances / metabolism
  • Xanthine Oxidase / metabolism*


  • Free Radicals
  • Thiobarbituric Acid Reactive Substances
  • Nitric Oxide Synthase
  • Xanthine Oxidase