Kako K J
Can J Cardiol. 1986 May-Jun;2(3):184-94.
This review begins with discussion concerning the effects of changes in phospholipid compositions on membrane functions. Next, pathogenetic mechanisms of ischemic cell damage are reviewed; a) membrane phospholipid breakdown, caused by the activation of phospholipases, as well as the intracellular Ca2+ overload, and b) univalent oxygen reduction and lipid peroxidation, probably all play important roles. Consequently, hydrophilic metabolites of lipid peroxidation may accumulate in the hydrophobic membrane bilayer during ischemia, causing membrane dysfunction. Free radicals may involve the cross-linking of membrane proteins as well. Previous results in support of the free radical hypothesis of myocardial ischemic injury are described; they were obtained from ESR studies, measurements of tissue antioxidants, determinations of lipid breakdown products, and studies using scavengers. The distribution, biosynthesis and physical-chemistry of plasmalogens are then discussed. Excepting the platelet activating factor recently discovered, only fragmentary information is available concerning the function of plasmalogens. It is possible that membrane plasmalogens, which contain large amounts of polyunsaturated fatty acids, are vulnerable to free radical/ischemic injury.
本综述首先讨论磷脂组成变化对膜功能的影响。接下来，回顾缺血性细胞损伤的发病机制；a）由磷脂酶激活以及细胞内钙超载引起的膜磷脂分解，以及b）一价氧还原和脂质过氧化，可能都起着重要作用。因此，脂质过氧化的亲水性代谢产物在缺血期间可能积聚在疏水膜双层中，导致膜功能障碍。自由基也可能参与膜蛋白的交联。描述了先前支持心肌缺血性损伤自由基假说的结果；这些结果来自电子自旋共振研究、组织抗氧化剂测量、脂质分解产物测定以及使用清除剂的研究。然后讨论了缩醛磷脂的分布、生物合成和物理化学性质。除了最近发现的血小板活化因子外，关于缩醛磷脂的功能只有零碎的信息。含有大量多不饱和脂肪酸的膜缩醛磷脂可能易受自由基/缺血性损伤。
