Delayed oxidative degradation of polyunsaturated diacyl phospholipids in the presence of plasmalogen phospholipids in vitro
Delayed oxidative degradation of polyunsaturated diacyl phospholipids in the presence of plasmalogen phospholipids in vitro
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DOI：
10.1042/bj3230807
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发表时间：
1997-05-01
影响因子：
4.1
通讯作者：
Engelmann, B
中科院分区：
文献类型：
--
作者：
Reiss, D;Beyer, K;Engelmann, B
在不存在和存在多不饱和酯磷脂的情况下，通过H-1-NMR和化学测定分析了缩醛磷脂（烯酰基）的氧化降解。在Triton X-100胶束（去污剂/磷脂1：5，mol/mol）中，用2，2 '-偶氮双-（2-脒基丙烷盐酸盐）（AAPH; 2或10 mM）氧化在sn（2）处含有增加数量的链内双键的脑溶血质乙醇胺（lyso-P-PE）、脑P-PE和红细胞P-PE。两个过氧自由基的形成是伴随着约降解。一分子的脑溶血磷脂在用2 mM AAPH氧化脑P-PE或红细胞P-PE（320 nmol）时，烯醇醚的（α-乙烯基）次甲基H-1信号比链内双键的次甲基质子峰下降得更快。烯醇醚降解速率依次为红细胞P-PE >脑P-PE >脑溶血P-PE。多不饱和酯磷脂1-棕榈酰-2-花生四烯酸磷脂酰胆碱（16：0/20：4-PC）和1-棕榈酰-2-亚油酰磷脂酰胆碱（16：0/18：2-PC）（100 nmol）的消失，由10 mM AAPH诱导，分别在孵育的前30和60 min几乎完全被缩醛磷脂（25 nmol）抑制，并在随后的时间点延迟。缩醛磷脂和维生素E（4-25 nmol）以类似的方式减轻了由2 mM AAPH诱导的16：0/[H-3]20：4-PC（100 nmol）的降低。16：0/20：4-PC和16：0/18：2-PC（320 nmol; 2 mM AAPH）的链内双键的初始降解速率在80 nmol脑lyso-P-PE存在下分别降低59%和81%。总之，缩醛磷脂在体外条件下显著延迟链内双键的氧化降解。烯醇醚双键与引发过氧自由基的相互作用以及与多不饱和脂肪酸氧化前产生的产物的相互作用被认为是缩醛磷脂这种能力的原因。此外，烯醇醚氧化的产物显然不会传播多不饱和脂肪酸的氧化。
The oxidative degradation of plasmalogen (alkenylacyl) phospholipids was analysed in the absence and the presence of polyunsaturated ester phospholipids by H-1-NMR and by chemical determination. Brain lysoplasmenylethanolamine (lyso-P-PE), brain P-PE and erythrocyte P-PE, containing an increasing number of intrachain double bonds at sn(2), were oxidized with 2,2'-azobis-(2-amidinopropane hydrochloride) (AAPH; 2 or 10 mM) in Triton X-100 micelles (detergent/phospholipid 1:5, mol/mol). The formation of two peroxyl radicals was accompanied by the degradation of approx. one molecule of brain lyso-P-PE. On oxidation of brain P-PE or erythrocyte P-PE(320 nmol) with 2 mM AAPH, the (alpha-vinyl) methine H-1 signal of the enol ether decreased more rapidly than the methine proton peak of intrachain double bonds. The rate of enol ether degradation increased in the order: erythrocyte P-PE > brain P-PE > brain lyso-P-PE. The disappearance of the polyunsaturated ester phospholipids 1-palmitoyl-2-arachidonoyl phosphatidylcholine (16:0/20:4-PC) and 1-palmitoyl-2-linoleoyl phosphatidylcholine (16:0/18:2-PC) (100 nmol), as induced by 10 mM AAPH, was nearly completely inhibited by the plasmalogens (25 nmol) in the first 30 and 60 min of incubation respectively, and was delayed at later time points. Plasmalogens and vitamin E (4-25 nmol) mitigated the decreases in 16:0/[H-3]20:4-PC (100 nmol) induced by 2 mM AAPH in a similar manner. The initial rate of degradation of intrachain double bonds of 16:0/20:4-PC and 16:0/18:2-PC (320 nmol; 2 mM AAPH) was decreased by 59 % and 81 % respectively in the presence of 80 nmol of brain lyso-P-PE. In conclusion, plasmalogens markedly delay the oxidative degradation of intrachain double bonds under in vitro conditions. Interactions of enol ether double bonds with initiating peroxyl radicals as well as with products generated by prior oxidation of polyunsaturated fatty acids are proposed to be responsible for this capacity of plasmalogens. Furthermore, the products of enol ether oxidation apparently do not propagate the oxidation of polyunsaturated fatty acids.