Department of Biochemistry, Lucknow University, Lucknow, India.
Med Sci Monit. 2009 Oct;15(10):RA209-219.
Oxidative stress is a condition in which reactive oxygen species (ROS) or free radicals, namely O2*(-), H2O2, and *OH, are generated extra- or intracellularly and exert toxic effects on cells. The heart is one of the major organs affected by ROS. Recent evidence suggests that oxidative stress is a common denominator in many aspects of cardiovascular diseases. During myocardial oxidative stress, the generation of ROS is enhanced and the defense mechanisms of myocytes are altered. The sources of ROS in cardiac myocytes could be mitochondrial electron transport chain, nitric oxide synthase (NOS), NADPH oxidase, xanthine oxidase, and lipoxygenase/cyclooxygenase and the auto-oxidation of various substances, particularly catecholamines. In acute myocardial infarction (AMI), two distinct types of damage occur to the heart: ischemic injury and reperfusion injury, which lead to mitochondrial dysfunction in heart cells. During ischemia and reperfusion, ROS can be produced by both endothelial cells and circulating phagocytes. Ischemia also causes alterations in the defense mechanisms against ROS. Some proteins, including heat-shock proteins, are overexpressed in conditions of ischemia/reperfusion and can protect from cardiac injury. This article outlines the current understanding of oxidative stress and ROS generation and their role in cardiovascular diseases, including ischemic myocardial syndromes. The following aspects are covered: oxidative stress, mitochondrial dysfunction and pathophysiological mechanisms of atherosclerosis, precipitation of MI, sources of ROS in cardiac myocytes, effects of ROS in the heart, and ischemia and reperfusion injuries and their mechanisms.
氧化应激是一种活性氧（ROS）或自由基（如 O2*(-)、H2O2 和 *OH）在细胞内外产生并对细胞产生毒性作用的状态。心脏是受 ROS 影响的主要器官之一。最近的证据表明，氧化应激是心血管疾病许多方面的共同因素。在心肌氧化应激期间，ROS 的产生增强，心肌细胞的防御机制发生改变。心肌细胞中 ROS 的来源可能包括线粒体电子传递链、一氧化氮合酶（NOS）、NADPH 氧化酶、黄嘌呤氧化酶和脂氧合酶/环加氧酶以及各种物质的自动氧化，特别是儿茶酚胺。在急性心肌梗死（AMI）中，心脏会发生两种不同类型的损伤：缺血性损伤和再灌注损伤，这会导致心肌细胞中线粒体功能障碍。在缺血和再灌注期间，ROS 可以由内皮细胞和循环吞噬细胞产生。缺血还会导致对 ROS 的防御机制发生改变。一些蛋白质，包括热休克蛋白，在缺血/再灌注条件下过度表达，可以保护心脏免受损伤。本文概述了目前对氧化应激和 ROS 产生及其在包括缺血性心肌综合征在内的心血管疾病中的作用的理解。涵盖的方面包括：氧化应激、线粒体功能障碍和动脉粥样硬化的病理生理机制、MI 的沉淀、心肌细胞中 ROS 的来源、ROS 对心脏的影响以及缺血和再灌注损伤及其机制。
