摘要
Free radicals contribute to the pathogenesis of both acute (ischemia—reperfusion injury) and chronic (atherosclerosis) cardiovascular diseases. This observation has led to the hypothesis that agents capable of inhibiting oxidative stress may be beneficial in the treatment of these diseases. In support of this hypothesis, prospective epidemiological studies have demonstrated a strong inverse relationship between serum antioxidant levels and the number of adverse events associated with coronary artery disease (CAD). The mechanistic rationale for this antioxidant benefit can be attributed to the “oxidative-modification hypothesis,” a model that proposes that certain inflammatory processes associated with atherogenesis are triggered by free radical-induced modification of lipids associated with low-density lipoproteins (LDL) and vascular cell membranes. Oxidative stress is also an important feature of heart failure; increasing levels of serum malondialdehyde, a product of lipid peroxidation, can be correlated with severity of disease. Thus, a better understanding of the mechanisms by which oxygen-based free radicals alter cell structure—function relationships could lead to the development of new treatments for cardiovascular disorders with greater efficacy and fewer side effects. This chapter discusses the basic mechanisms by which free radicals effect cell injury and the potential role for compounds with antioxidant activity to intervene in these disease processes.
摘要译文
自由基有助于急性（缺血 - 再灌注损伤）和慢性（动脉粥样硬化）心血管疾病的发病机制。该观察结果导致了这样的假设：能够抑制氧化应激的药剂可能有益于治疗这些疾病。为了支持这个假设，前瞻性流行病学研究表明血清抗氧化水平与冠状动脉疾病（CAD）相关的不良事件数量之间存在强烈的反比关系。这种抗氧化作用的机理原理可以归结为“氧化修饰假说，通过自由基诱导的与低密度脂蛋白（LDL）和血管细胞膜相关的脂质的修饰，引发与动脉粥样化形成相关的某些炎症过程。氧化应激也是心力衰竭的重要特征;血清丙二醛（脂质过氧化产物）水平的增加可与疾病的严重程度相关联。从而，基于氧的自由基改变细胞结构 - 功能关系可能导致心血管疾病的新疗法的开发，具有更大的功效和更少的副作用。本章讨论了自由基影响细胞损伤的基本机制以及具有抗氧化活性的化合物干预这些疾病过程的潜在作用。
R. Preston Mason. Role of Antioxidants in Coronary Artery Disease. Preventive Cardiology[M].DE: Springer, 2001: 29-45