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
            
    
