Esterbauer H, Wäg G, Puhl H
Institute of Biochemistry, University of Graz, Austria.
Br Med Bull. 1993 Jul;49(3):566-76. doi: 10.1093/oxfordjournals.bmb.a072631.
A crucial step in the pathogenesis of atherosclerosis is believed to be the oxidative modification of low density lipoprotein (LDL). The oxidation of LDL is a free radical driven lipid peroxidation process and the aldehyde products of lipid hydroperoxide breakdown are responsible for the modification of the LDL apoprotein. Aldehyde-modified apoB protein has altered receptor affinity, causing it to be scavenged by macrophages in an uncontrolled manner with the development of foam cells and the initiation of the atherosclerotic lesion. The aldehydic products of lipid peroxidation may also be involved in other aspects of the development of the lesion. The oxidation of LDL may be prevented by its endogenous antioxidant compounds, most prominent of which is alpha-tocopherol. Consequently, an improved antioxidant status may offer possibilities for the prevention of this major disease.
动脉粥样硬化发病机制中的一个关键步骤被认为是低密度脂蛋白（LDL）的氧化修饰。LDL的氧化是一个由自由基驱动的脂质过氧化过程，脂质过氧化氢分解产生的醛类产物负责修饰LDL载脂蛋白。醛修饰的载脂蛋白B蛋白改变了受体亲和力，导致其被巨噬细胞以不受控制的方式清除，从而形成泡沫细胞并引发动脉粥样硬化病变。脂质过氧化的醛类产物也可能参与病变发展的其他方面。LDL的氧化可以通过其内源性抗氧化化合物来预防，其中最主要的是α-生育酚。因此，改善抗氧化状态可能为预防这种主要疾病提供可能性。
