Coetzee I H, Lochner A
Department of Medical Physiology and Biochemistry, Faculty of Medicine, University of Stellenbosch, Tygerberg, Republic of South Africa.
Cardioscience. 1993 Dec;4(4):205-15.
Previous studies have shown that myocardial membranes, isolated from ischemic myocardial tissue, showed marked changes in microviscosity. To evaluate the contribution of free radical production and concomitant lipid peroxidation to these changes in microviscosity, the in vitro effects of two radical producing systems (H2O2/FeCl2 and xanthine oxidase/hypoxanthine/FeCl3) were investigated separately on the microviscosity of sarcolemmal, mitochondrial and sarcoplasmic reticulum membranes. In all three membranes both these free radical producing systems caused formation of malondialdehyde as quantitated by the thiobarbituric acid test. The sensitivity of the membranes to free radical damage differed: the sarcolemma was more sensitive to H2O2 damage, while mitochondrial malondialdehyde production was highest with xanthine oxidase. H2O2/FeCl2 caused a reduction in microviscosity (i.e. increased fluidity) of all three membranes, whereas the xanthine oxidase system increased mitochondrial and sarcolemmal microviscosity and reduced that of the sarcoplasmic reticulum. The similarity between ischemia-induced membrane microviscosity changes and those induced in vitro by xanthine oxidase, indicate a possible causal role for superoxide and hydroxyl free radicals produced during ischemia.
先前的研究表明，从缺血心肌组织中分离出的心肌膜在微粘度方面表现出显著变化。为了评估自由基产生及伴随的脂质过氧化对这些微粘度变化的影响，分别研究了两种自由基产生系统（过氧化氢/氯化亚铁和黄嘌呤氧化酶/次黄嘌呤/氯化铁）对肌膜、线粒体膜和肌浆网膜微粘度的体外作用。在这三种膜中，通过硫代巴比妥酸试验定量分析发现，这两种自由基产生系统均导致了丙二醛的形成。不同膜对自由基损伤的敏感性有所不同：肌膜对过氧化氢损伤更为敏感，而黄嘌呤氧化酶作用下线粒体丙二醛的生成量最高。过氧化氢/氯化亚铁导致所有三种膜的微粘度降低（即流动性增加），而黄嘌呤氧化酶系统则增加了线粒体膜和肌膜的微粘度，降低了肌浆网膜的微粘度。缺血诱导的膜微粘度变化与黄嘌呤氧化酶体外诱导的变化之间的相似性，表明缺血期间产生的超氧阴离子和羟自由基可能具有因果作用。
