Gottlieb Roberta A
Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 N. Torrey Pines Road MEM220, La Jolla, CA 92037, USA.
Arch Biochem Biophys. 2003 Dec 15;420(2):262-7. doi: 10.1016/j.abb.2003.07.004.
While attention has historically focused on mitochondria as the primary source of ROS in myocardial ischemia/reperfusion injury, recent evidence has implicated cytochrome P450 monooxygenases (CYPs) as a significant factor. CYPs represent a large family of enzymes that catalyze the oxidation of endogenous and exogenous compounds. They catalyze arachidonic acid oxidation to a variety of biologically active eicosanoids that regulate ion channels and protein kinases, with effects on vasomotor tone and cardiac inotropy. They also represent a significant source of reactive oxygen species that may target cellular homeostatic mechanisms and mitochondria. In this review, we will consider the contribution of cytochrome P450 enzymes to reperfusion injury and will speculate on whether the mechanism of injury is due to CYP-mediated ROS production or arachidonic acid metabolites.
虽然历史上注意力一直集中在线粒体是心肌缺血/再灌注损伤中活性氧（ROS）的主要来源，但最近的证据表明细胞色素P450单加氧酶（CYPs）是一个重要因素。CYPs是一大类催化内源性和外源性化合物氧化的酶。它们催化花生四烯酸氧化生成多种调节离子通道和蛋白激酶的生物活性类二十烷酸，对血管舒缩张力和心脏收缩力产生影响。它们也是活性氧的重要来源，可能靶向细胞内稳态机制和线粒体。在这篇综述中，我们将探讨细胞色素P450酶对再灌注损伤的作用，并推测损伤机制是由于CYP介导的ROS产生还是花生四烯酸代谢产物。
