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Articles in PresS, published online ahead of print October 17, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00581.2002
Submitted on July 12, 2002
Accepted on October 4, 2002
Increases Production of Hydroxyl Radical in Murine Myocardium
1 Department of Cardiovascular Medicine, Kyushu University, Graduate School of Medical Sciences, Fukuoka, Japan
2 Department of Biophysics, Kyushu University, Graduate School of Pharmaceutical Sciences, Fukuoka, Japan
3 Cardiovascular Institute, University of Pittsburgh Medical Center, Pittsburgh, USA
* To whom correspondence should be addressed. E-mail: kubotat{at}cardiol.med.kyushu-u.ac.jp.
Transgenic mice with cardiac-specific overexpression of tumor necrosis factor-
(TG) develop congestive heart failure with myocardial inflammation. The purpose of this study was to investigate the effects of tumor necrosis factor- on reactive oxygen species (ROS) in this mouse model of cardiomyopathy. Myocardial production of hydroxyl radical detected by electron spin resonance spectroscopy was significantly increased in TG. Myocardial expression of Mn-SOD was significantly decreased in TG, while that of Cu/Zn-SOD was unaltered. Myocardial expression of catalase was unchanged, whereas that of glutathione peroxidase was significantly increased in TG. Histological analysis revealed that macrophages and CD4-positive lymphocytes were increased in TG myocardium. To investigate whether these infiltrating inflammatory cells were the source of ROS, we treated TG with cyclophosphamide for seven days. Although cyclophosphamide significantly suppressed the infiltration of inflammatory cells, it did not diminish the production of hydroxyl radical in TG myocardium. Damaged myocytes, but not infiltrating inflammatory cells, may be the source of ROS in transgenic mice with cardiac-specific overexpression of tumor necrosis factor-.
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