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亚油酸过氧化——低密度脂蛋白中主要的脂质过氧化过程——及其与慢性疾病的关系。

Linoleic acid peroxidation--the dominant lipid peroxidation process in low density lipoprotein--and its relationship to chronic diseases.

作者信息

Spiteller G

机构信息

Lehrstuhl Organische Chemie I, Universität Bayreuth, Germany.

出版信息

Chem Phys Lipids. 1998 Oct;95(2):105-62. doi: 10.1016/s0009-3084(98)00091-7.

DOI:10.1016/s0009-3084(98)00091-7
PMID:9853364
Abstract

Modern separation and identification methods enable detailed insight in lipid peroxidation (LPO) processes. The following deductions can be made: (1) Cell injury activates enzymes: lipoxygenases generate lipid hydroperoxides (LOOHs), proteases liberate Fe ions--these two processes are prerequisites to produce radicals. (2) Radicals attack any activated CH2-group of polyunsaturated fatty acids (PUFAs) with about a similar probability. Since linoleic acid (LA) is the most abundant PUFA in mammals, its LPO products dominate. (3) LOOHs are easily reduced in biological surroundings to corresponding hydroxy acids (LOHs). LOHs derived from LA, hydroxyoctadecadienoic acids (HODEs), surmount other markers of LPO. HODEs are of high physiological relevance. (4) In some diseases characterized by inflammation or cell injury HODEs are present in low density lipoproteins (LDL) at 10-100 higher concentration, compared to LDL from healthy individuals.

摘要

现代分离和鉴定方法能够深入洞察脂质过氧化(LPO)过程。可以得出以下推论:(1)细胞损伤会激活酶:脂氧合酶生成脂质氢过氧化物(LOOHs),蛋白酶释放铁离子——这两个过程是产生自由基的先决条件。(2)自由基以大致相似的概率攻击多不饱和脂肪酸(PUFAs)的任何活化CH2基团。由于亚油酸(LA)是哺乳动物中最丰富的多不饱和脂肪酸,其LPO产物占主导地位。(3)LOOHs在生物环境中很容易还原为相应的羟基酸(LOHs)。源自LA的LOHs,即羟基十八碳二烯酸(HODEs),超过了LPO的其他标志物。HODEs具有高度的生理相关性。(4)在一些以炎症或细胞损伤为特征的疾病中,与健康个体的低密度脂蛋白(LDL)相比,HODEs在低密度脂蛋白中的浓度高出10至100倍。

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