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increases
production of hydroxyl radical in murine myocardium
1 Department of Cardiovascular Medicine, Graduate School of Medical Sciences, and 2 Department of Biophysics, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan; and 3 Cardiovascular Institute, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213
Transgenic (TG) mice with
cardiac-specific overexpression of tumor necrosis factor-
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, whereas 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 mice with cyclophosphamide for 7 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 TG.
cytokine; heart failure; reactive oxygen species
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