Kerckaert I, Roels F
Basic Res Cardiol. 1986 Jan-Feb;81(1):83-91. doi: 10.1007/BF01907430.
Myocardial H2O2 production was studied by means of the in vivo administration of aminotriazole (AT), which inactivates the catalase-H2O2 complex compound I. Measurements of the residual catalase activity in male and female rats indicate that beta-oxidation of fatty acids in peroxisomes does not contribute in a substantial way to energy production in response to fasting or to an increased myocardial load, despite previous data on peroxisomes in myocardium. Superoxide dismutase (SOD) inhibition by diethyldithiocarbamate demonstrates that SOD participates in the production of H2O2 in physiological conditions. Such a role was not demonstrated for monoamine oxidase through inhibition by phenelzine.
通过体内给予氨基三唑（AT）来研究心肌过氧化氢（H₂O₂）的产生，氨基三唑可使过氧化氢酶-H₂O₂复合化合物I失活。对雄性和雌性大鼠残余过氧化氢酶活性的测量表明，尽管之前有关于心肌过氧化物酶体的数据，但过氧化物酶体中脂肪酸的β氧化对禁食或心肌负荷增加时的能量产生贡献不大。二乙基二硫代氨基甲酸盐对超氧化物歧化酶（SOD）的抑制作用表明，SOD在生理条件下参与H₂O₂的产生。通过苯乙肼抑制单胺氧化酶并未证明其有这样的作用。
