Wilhelm J
Third Medical Clinic, First Medical Faculty, Charles University, Prague, Czechoslovakia.
Acta Univ Carol Med Monogr. 1990;137:1-53.
Lipid peroxidation is a free radical initiated chain oxidation of unsaturated lipids. With respect to the ubiquity of unsaturated fatty acids in the cellular membranes, the peroxidative damage has the potential to affect many cellular functions. Some of the products of lipid peroxidation are diffusible and can spread the damage far beyond the site of the original free radical attack. There is an interdependency between reactive oxygen species and lipid peroxidation - reactive oxygen species initiate the reactions of lipid peroxidation and are also produced in these reactions as intermediates. The generation of reactive oxygen species can be triggered either by nonenzymatic mechanisms, in which iron ions play the major role, or by a wide range of enzymatic systems. The primary damaging effect of lipid peroxidation is exerted by the interactions with proteins and DNA. These interactions are then revealed at the subcellular (cellular organelles), cellular, and organ levels. The production of lipid peroxides interferes with the regulation of several metabolic pathways. In this review, particular attention is focused on the interaction of non-specifically formed lipid peroxides with the regulatory factors produced by the controlled oxidation of arachidonic acid (prostaglandins and leukotrienes), the effects on ionic pumps and intracellular calcium metabolism, the participation of lipid peroxidation in the ageing process, and the modulation of hormonal regulations by lipid peroxidation. Lipid peroxidation is induced at the level of the whole organism by various extrinsic factors such as ionizing irradiation, physical activity, diet and fasting, and various drugs. There is increasing awareness of the association between pathologic states and lipid peroxidation. Among the most studied are inflammation, ischaemia-reperfusion injury, and atherogenesis. Lipid peroxidation also plays a dual and complex role in cancer. Organisms have developed an efficient multilevel protective system against lipid peroxidation, but this can be overwhelmed by certain pathologies.
脂质过氧化是自由基引发的不饱和脂质的链式氧化反应。鉴于不饱和脂肪酸在细胞膜中广泛存在，过氧化损伤有可能影响多种细胞功能。脂质过氧化的一些产物具有扩散性，能够将损伤传播到远离最初自由基攻击的部位。活性氧与脂质过氧化之间存在相互依存关系——活性氧引发脂质过氧化反应，并且在这些反应中作为中间体产生。活性氧的产生可由非酶机制触发，其中铁离子起主要作用，也可由多种酶系统触发。脂质过氧化的主要损伤作用是通过与蛋白质和DNA的相互作用来发挥的。这些相互作用随后在亚细胞（细胞器）、细胞和器官水平上显现出来。脂质过氧化物的产生会干扰多种代谢途径的调节。在本综述中，特别关注非特异性形成的脂质过氧化物与花生四烯酸受控氧化产生的调节因子（前列腺素和白三烯）之间的相互作用、对离子泵和细胞内钙代谢的影响、脂质过氧化在衰老过程中的作用以及脂质过氧化对激素调节的影响。脂质过氧化在整个生物体水平上可由各种外部因素诱导，如电离辐射、体育活动、饮食和禁食以及各种药物。人们越来越意识到病理状态与脂质过氧化之间的关联。研究最多的是炎症、缺血再灌注损伤和动脉粥样硬化的形成。脂质过氧化在癌症中也起着双重且复杂的作用。生物体已经发展出一种高效的多层次脂质过氧化保护系统，但某些病理状态可能会使其不堪重负。
