Heinecke J W
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Biofactors. 1997;6(2):145-55. doi: 10.1002/biof.5520060208.
Many lines of evidence implicate oxidation of low density lipoprotein (LDL) in the pathogenesis of atherosclerosis, a chronic inflammatory disease. The physiologically relevant mechanisms have not been identified, but phagocytic white cells may play an important role because macrophage-rich lesions characterize the disorder. Recent studies have shown that myeloperoxidase, a heme enzyme secreted only by phagocytes, is present in human atherosclerotic tissue. The enzyme is a potent catalyst of LDL oxidation in vitro, it co-localizes with macrophages in lesions, and it generates products that are detectable in atherosclerotic plaque. These findings suggest that myeloperoxidase may promote LDL oxidation in the artery wall. This article reviews the enzyme's ability to generate a range of oxidants, including tyrosyl radical, reactive aldehydes, hypochlorous acid and molecular chlorine. These products have the potential to damage host molecules as well as microbes, suggesting a mechanism that may contribute to atherosclerotic vascular disease.
多条证据表明，低密度脂蛋白（LDL）氧化与动脉粥样硬化（一种慢性炎症性疾病）的发病机制有关。生理相关机制尚未明确，但吞噬性白细胞可能起重要作用，因为富含巨噬细胞的病变是该疾病的特征。最近的研究表明，髓过氧化物酶（一种仅由吞噬细胞分泌的血红素酶）存在于人类动脉粥样硬化组织中。该酶在体外是LDL氧化的有效催化剂，它与病变中的巨噬细胞共定位，并且能产生在动脉粥样硬化斑块中可检测到的产物。这些发现表明髓过氧化物酶可能促进动脉壁中的LDL氧化。本文综述了该酶产生一系列氧化剂的能力，包括酪氨酰自由基、活性醛、次氯酸和分子氯。这些产物有可能损害宿主分子以及微生物，提示了一种可能导致动脉粥样硬化性血管疾病的机制。
