Wykle R L, Schremmer Lockmiller J M
Biochim Biophys Acta. 1975 Feb 20;380(2):291-8. doi: 10.1016/0005-2760(75)90015-6.
The biosynthesis of 1-alk-1'-enyl-2-acyl-sn-glycero-3-phosphoethanolamine (ethanolamine plasmalogens) was studied using 1-[1-14C]hexadecyl-sn-glycero-3-phosphoethanolamine as the substrate and EDTA-washed microsomes from brains of 14-day-old rats. It was found that the 1-E11-14C]hexadecyl-sn-glycero-3-phosphoethanolamine was first acylated to form 1-[1-14C]hexadecyl-2-acyl-sn-glycero-3-phosphoethanolamine, then was desaturated to form 1-[1-14C]hexadec-1'-enyl-2-acyl-sn-glycero-3-phosphoethanolamine. The desaturation required O2 and NADH or NADPH and was inhibited by KCN but not by CO. The data indicated that the desaturation is carried out by a mixed-function oxidase system similar to that involved in the desaturation of fatty acids and that the pathway for the biosynthesis of plasmalogens in brain is similar to that previously found in other tissues. The desaturase was not stimulated by ATP and Mg2plus nor inhibited by EDTA. The specific activity of microsomes from brains of rats of different ages was determined; the activity decreased with age until in adults the activity was only 15% that of the 12--14-day-old rats.
以1-[1-¹⁴C]十六烷基-sn-甘油-3-磷酸乙醇胺为底物，使用14日龄大鼠脑的EDTA洗涤微粒体，研究了1-烯基-2-酰基-sn-甘油-3-磷酸乙醇胺（乙醇胺缩醛磷脂）的生物合成。结果发现，1-[1-¹⁴C]十六烷基-sn-甘油-3-磷酸乙醇胺首先被酰化形成1-[1-¹⁴C]十六烷基-2-酰基-sn-甘油-3-磷酸乙醇胺，然后去饱和形成1-[1-¹⁴C]十六-1'-烯基-2-酰基-sn-甘油-3-磷酸乙醇胺。去饱和需要氧气和NADH或NADPH，并且被KCN抑制但不被CO抑制。数据表明，去饱和是由类似于脂肪酸去饱和过程中涉及的混合功能氧化酶系统进行的，并且脑中缩醛磷脂的生物合成途径与先前在其他组织中发现的途径相似。去饱和酶不受ATP和Mg²⁺刺激，也不受EDTA抑制。测定了不同年龄大鼠脑微粒体的比活性；活性随年龄下降，直到成年时活性仅为12 - 14日龄大鼠的15%。
