Reiss D, Beyer K, Engelmann B
Physiologisches Institut der Universität München, Pettenkoferstr. 12, D-80336 München, Germany.
Biochem J. 1997 May 1;323 ( Pt 3)(Pt 3):807-14. doi: 10.1042/bj3230807.
The oxidative degradation of plasmalogen (alkenylacyl) phospholipids was analysed in the absence and the presence of polyunsaturated ester phospholipids by 1H-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 sn2, 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 1H 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/[3H]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.
通过1H-NMR和化学测定法，在不存在和存在多不饱和酯磷脂的情况下，分析了缩醛磷脂（烯基酰基）磷脂的氧化降解。脑溶血缩醛磷脂酰乙醇胺（溶血-P-PE）、脑P-PE和红细胞P-PE在sn2位含有数量不断增加的链内双键，在Triton X-100胶束（去污剂/磷脂1:5，摩尔/摩尔）中用2,2'-偶氮双（2-脒基丙烷盐酸盐）（AAPH；2或10 mM）进行氧化。两个过氧自由基的形成伴随着约一分子脑溶血-P-PE的降解。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1H信号比链内双键的次甲基质子峰下降得更快。烯醇醚降解速率按以下顺序增加：红细胞P-PE>脑P-PE>脑溶血-P-PE。10 mM AAPH诱导的多不饱和酯磷脂1-棕榈酰-2-花生四烯酰磷脂酰胆碱（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，在前30分钟和60分钟的孵育中分别几乎完全被缩醛磷脂（25 nmol）抑制，并且在随后的时间点延迟。缩醛磷脂和维生素E（4-25 nmol）以类似方式减轻了2 mM AAPH诱导的16:0/[3H]20:4-PC（100 nmol）的减少。在存在80 nmol脑溶血-P-PE的情况下，16:0/20:4-PC和16:0/18:2-PC（320 nmol；2 mM AAPH）链内双键的初始降解速率分别降低了59%和81%。总之，在体外条件下，缩醛磷脂显著延迟了链内双键的氧化降解。烯醇醚双键与引发过氧自由基以及与多不饱和脂肪酸先前氧化产生的产物之间的相互作用被认为是缩醛磷脂具有这种能力的原因。此外，烯醇醚氧化产物显然不会促进多不饱和脂肪酸的氧化。
