Increased xanthine oxidase activity after traumatic brain injury in rats.
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.
Solaroglu
Ihsan
I
Department of Neurological Surgery, Ankara Numune Research and Education Hospital, Ankara, Turkey. isolaroglu@hotmail.com
Okutan
Ozerk
O
Kaptanoglu
Erkan
E
Beskonakli
Etem
E
Kilinc
Kamer
K
D000818:Animals; D001921:Brain / Q000201:enzymology; D001930:Brain Injuries / Q000201:enzymology* / Q000473:pathology; D003593:Cytoplasm / Q000201:enzymology; D005609:Free Radicals / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D019001:Nitric Oxide Synthase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014969:Xanthine Oxidase / Q000378:metabolism*
D005609:Free Radicals; D017392:Thiobarbituric Acid Reactive Substances; D019001:Nitric Oxide Synthase; D014969:Xanthine Oxidase