Kawamura Yoshikatsu
Affiliate Master
Yamaguchi University
Xanthine oxidase is one of the major sources of superoxide anion radicals in blood after reperfusion in rats with forebrain ischemia/reperfusion
Brain research : international multidisciplinary journal devoted to fundamental research in the brain sciences Volume 1305
Page 158-167
published_at 2009-12-11
Title
Xanthine oxidase is one of the major sources of superoxide anion radicals in blood after reperfusion in rats with forebrain ischemia/reperfusion
Creators
Shinagawa Aki Hiromi
Creators
Wakatsuki Jun
Creators
Aoki Tetsuya
Creators
Kobayashi Chihiro
Creators
Kasaoka Shunji
Creators
Maruyama Ikuro
Creators
Yuasa Makoto
Creator Keywords
allopurinol
electrochemical sensor
forebrain ischemia
reperfusion
superoxide anion radical
xanthine oxidase inhibitor
We recently reported that excessive superoxide anion radical (O_2–•) was generated in the jugular vein during reperfusion in rats with forebrain ischemia-reperfusion using a novel electrochemical sensor and excessive O_2–• generation was associated with oxidative stress, early inflammation, and endothelial injury. However, the source of O_2–• was still unclear. Therefore, we used allopurinol, a potent inhibitor of xanthine oxidase (XO), to clarify the source of O_2–• generated in rats with forebrain ischemia-reperfusion. The increased O_2–• current and the quantified partial value of electricity (Q), which was calculated by the integration of the current, were significantly attenuated after reperfusion by pretreatment with allopurinol. Malondialdehyde (MDA) in the brain and plasma, High-mobility group box 1 (HMGB1) in plasma, and intercellular adhesion molecule-1 (ICAM-1) in the brain and plasma were significantly attenuated in rats pretreated with allopurinol with dose-dependency in comparison to those in control rats. There were significant correlations between total Q and MDA, HMGB, or ICAM-1 in the brain and plasma. Allopurinol pretreatment suppressed O_2–• generation in the brain-perfused blood in the jugular vein, and oxidative stress, early inflammation, and endothelial injury in the acute phase of forebrain ischemia-reperfusion. Thus, XO is one of the major sources of O_2–• in blood after reperfusion in rats with forebrain ischemia-reperfusion.
Languages
eng
Resource Type
journal article
Publishers
Elsevier
Date Issued
2009-12-11
Rights
Copyright c2009 Elsevier Inc. All rights reserved.()
File Version
Author’s Original
Access Rights
open access
Relations
[ISSN]0006-8993
[NCID]AA0057324X
[PMID]info:pmid/19781528
[isVersionOf]
[URI]http://www.sciencedirect.com/science/journal/00068993