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ID 54416
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Setiawan, Heri Department of Public Health, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Nagaoka, Kenjiro Department of Public Health, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kubo, Masayuki Department of Public Health, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Fujikura, Yoshihisa Division of Morphological Analysis, Department of Anatomy, Biology and Medicine, Faculty of Medicine, Oita University
Ogino, Keiki Department of Public Health, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Abstract
Oxidative stress is widely known to play a role in asthma. However, the contribution of xanthine oxidoreductase (XOR) as a source of the superoxide anion radical (O2-) in oxidative stress associated with asthma has not yet been examined in detail. Here we investigated pathophysiological changes in XOR in an experimental model of asthma induced by the house dust mite Dermatophagoides farinae (Df). In the lungs of Df-treated mice, the production of O2- from XOR increased and the nitrite concentrations decreased, whereas the protein expression of XOR remained unchanged. Moreover, the protein expression levels of XOR and the hydrogen peroxide (H2O2) concentrations in bronchoalveolar lavage fluid (BALF) were higher in the Df-treated mice than in saline-treated mice. Immunohistochemically, although XOR was highly localized in the bronchial epithelial cells of the saline-treated mice, immunostaining for XOR was absent in the bronchial epithelium of Df-treated mice. These results suggest that oxidative stress is up-regulated by increases in the conversion of the dehydrogenase form (xanthine dehydrogenase; XDH) of XOR to the oxidase form (xanthine oxidase; XOD).
Keywords
xanthine oxidase
oxidative stress
asthma
Amo Type
Original Article
Published Date
2016-06
Publication Title
Acta Medica Okayama
Volume
volume70
Issue
issue3
Publisher
Okayama University Medical School
Start Page
175
End Page
182
ISSN
0386-300X
NCID
AA00508441
Content Type
Journal Article
language
英語
Copyright Holders
CopyrightⒸ 2016 by Okayama University Medical School
File Version
publisher
Refereed
True
PubMed ID
Web of Science KeyUT