Natarajan V, Schmid P C, Schmid H H
Biochim Biophys Acta. 1986 Aug 14;878(1):32-41. doi: 10.1016/0005-2760(86)90341-3.
N-Acylethanolamine phospholipids accumulate in rat brain during post-decapitative ischemia. Small amounts of these phospholipids consisting primarily of diacyl and alkenylacyl species can be detected within 15 min of ischemia and they increase linearly for 60 min. This ischemia-induced synthesis is more pronounced in developing rat brain (approx. 5.0 nmol/h per mumol lipid P) than in adult brain (0.4 nmol). Pulse labeling experiments with subcellular preparations of 10-day-old rat brain indicate a precursor-product relationship between ethanolamine phospholipids and their N-acyl analogs. N-Acylation of endogenous substrates occurs with both microsomes and mitochondria, exhibits a pH optimum of 10 and requires 1 mM Ca2+ for maximal (0.2 mM Ca2+ for half maximal) activity. Cell-free preparations of both developing and adult rat brain contain a phosphodiesterase which hydrolyzes N-acylphosphatidylethanolamine to phosphatidic acid and N-acylethanolamine. The latter is further hydrolyzed to fatty acid and ethanolamine by an amidohydrolase. [1-3H]Ethanolamine, injected intracerebrally or intraperitoneally into 13- and 18-day-old rats, is incorporated into brain ethanolamine phospholipids. Since small amounts of radioactivity are also associated with N-acylethanolamine phospholipids 5 and 24 h after injection of the substrate, it appears that these phospholipids may occur at a very low level as a natural lipid constituent of rat brain.
N-酰基乙醇胺磷脂在断头后缺血期间在大鼠脑中蓄积。在缺血15分钟内即可检测到少量主要由二酰基和烯基酰基种类组成的这些磷脂，并且它们在60分钟内呈线性增加。这种缺血诱导的合成在发育中的大鼠脑（约5.0 nmol/h每微摩尔脂质P）中比在成年脑中（0.4 nmol）更明显。用10日龄大鼠脑的亚细胞制剂进行的脉冲标记实验表明乙醇胺磷脂与其N-酰基类似物之间存在前体-产物关系。内源性底物的N-酰化作用在微粒体和线粒体中均会发生，最适pH为10，最大活性需要1 mM Ca2+（半最大活性需要0.2 mM Ca2+）。发育中和成年大鼠脑的无细胞制剂均含有一种磷酸二酯酶，可将N-酰基磷脂酰乙醇胺水解为磷脂酸和N-酰基乙醇胺。后者被酰胺水解酶进一步水解为脂肪酸和乙醇胺。向13日龄和18日龄大鼠脑内或腹腔内注射[1-3H]乙醇胺后，其会掺入脑乙醇胺磷脂中。由于在注射底物后5小时和24小时，少量放射性也与N-酰基乙醇胺磷脂相关，因此这些磷脂似乎可能以非常低的水平作为大鼠脑的天然脂质成分存在。
