Lenzen S, Görlich J K, Rustenbeck I
Institute of Pharmacology and Toxicology, University of Göttingen, F.R.G.
Biochim Biophys Acta. 1989 Jun 26;982(1):140-6. doi: 10.1016/0005-2736(89)90184-3.
Lysophospholipids inhibited mitochondrial Ca2+ uptake, induced a net Ca2+ efflux, and thereby increased the extramitochondrial Ca2+ concentration. The inhibitory potency decreased in the order lysophosphatidylcholine (LPC) = lysophosphatidylglycerol (LPG) greater than lysophosphatidylinositol (LPI) greater than lysophosphatidylserine (LPS) much greater than lysophosphatidylethanolamine (LPE). This relative order is in inverse relation to the ability of the various phospholipid head-groups to build up intermolecular hydrogen bonds with neighbouring membrane lipids. This indicates that changes in Ca2+ transport induced by lysophospholipids are mediated by the interaction of the lysophospholipids with the mitochondrial membrane bilayer structure. The mitochondrial membrane potential, which is the main driving force for mitochondrial Ca2+ uptake, was affected in the same order by the various lysophospholipids. This reduction of the mitochondrial membrane potential may be the underlying cause for the inhibition of the mitochondrial Ca2+ uniport and the resulting release of Ca2+ from the mitochondria.
溶血磷脂抑制线粒体对钙离子的摄取，诱导钙离子净流出，从而增加线粒体外钙离子浓度。抑制效力的顺序为溶血磷脂酰胆碱（LPC）=溶血磷脂酰甘油（LPG）＞溶血磷脂酰肌醇（LPI）＞溶血磷脂酰丝氨酸（LPS）＞＞溶血磷脂酰乙醇胺（LPE）。这种相对顺序与各种磷脂头部基团与相邻膜脂形成分子间氢键的能力呈反比。这表明溶血磷脂诱导的钙离子转运变化是由溶血磷脂与线粒体膜双层结构的相互作用介导的。线粒体膜电位是线粒体摄取钙离子的主要驱动力，受到各种溶血磷脂相同顺序的影响。线粒体膜电位的这种降低可能是抑制线粒体钙离子单向转运以及导致钙离子从线粒体释放的根本原因。
