Thayer W S
FEBS Lett. 1986 Jun 23;202(1):137-40. doi: 10.1016/0014-5793(86)80664-0.
Cardiac metabolism of H2O2 was studied by determining the concentration dependence for H2O2-stimulated release of GSSG, an indicator for flux through the glutathione peroxidase pathway, in perfused heart preparations. Treatment of rats with aminotriazole in vivo inhibited heart catalase by 83% and shifted the dose-response curve for GSSG release toward lower H2O2 concentrations. In aminotriazole-treated rats, 50 microM H2O2 elicited a maximal rate of GSSG release (about 5 nmol GSSG/min per g heart), whereas 200 microM H2O2 was necessary for obtaining a similar rate of GSSG release in control rat hearts. The results show that catalase, although present at low levels of activity in the heart compared to other organs, functions as a major route for detoxication of H2O2 in the myocardium.
通过测定灌注心脏标本中谷胱甘肽过氧化物酶途径通量指标——谷胱甘肽二硫化物（GSSG）的释放对过氧化氢（H2O2）刺激的浓度依赖性，研究了心脏对H2O2的代谢情况。体内用氨基三唑处理大鼠可使心脏过氧化氢酶活性抑制83%，并使GSSG释放的剂量反应曲线向较低H2O2浓度偏移。在氨基三唑处理的大鼠中，50微摩尔/升的H2O2引发了最大的GSSG释放速率（约为每克心脏每分钟5纳摩尔GSSG），而在对照大鼠心脏中，需要200微摩尔/升的H2O2才能获得类似的GSSG释放速率。结果表明，过氧化氢酶虽然与其他器官相比在心脏中的活性水平较低，但却是心肌中H2O2解毒的主要途径。
