PATHWAYS FOR OXIDATION OF LOW DENSITY LIPOPROTEIN BY MYELOPEROXIDASE

许多证据表明低密度的氧化作用 脂蛋白(LDL)在动脉粥样硬化发病机制中的作用 炎症性疾病。生理上相关的机制有 未被确认，但吞噬的白细胞可能起重要作用 因为巨噬细胞丰富的病变是这种疾病的特征。这 文章回顾了这种酶产生一系列氧化剂的能力， 包括酪氨酸基、反应性醛、次氯酸和 分子氯。这些产品有可能损害宿主 分子和微生物，暗示了一种可能 导致动脉粥样硬化性血管疾病。

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. 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.