Edgar A D, Strosznajder J, Horrocks L A
J Neurochem. 1982 Oct;39(4):1111-6. doi: 10.1111/j.1471-4159.1982.tb11503.x.
Extracts of acetone-dried powders from ischemic gerbil brain were examined for phospholipase A1 and A2 activities with phosphatidylethanolamine at pH 7.2. Ischemia was induced by bilateral ligation, and the animals were killed by immersion into liquid nitrogen. Bilateral ligation with ketamine as general anesthetic resulted in a rapid, transient increase in phospholipase A2 activity. The activity increased from 0.46 nmol/h/mg protein at 0 time to 0.82 nmol/h/mg protein at 1 min of ligation. Phospholipase A1 activity also increased from 0.7 go 1.3 nmol/h/mg protein within the 1st min. When Nembutal was used as anesthetic, the phospholipase activation was earlier, within the first 30 s. Similar results were found for ischemia induced by decapitation of Wistar rats without anesthesia. Bilateral ligation of the carotid arteries of the gerbil is known to increase the concentration of free fatty acids, particularly arachidonate. This increase is, at least in part, due to phospholipase A activation. As ethanolamine phospholipase A2 in brain does not require Ca2+ for activity, these results suggest that phospholipase A2 activation in ischemic brain results from a covalent modification of the enzyme.
用磷脂酰乙醇胺在pH 7.2条件下检测缺血沙土鼠脑丙酮干粉提取物的磷脂酶A1和A2活性。缺血通过双侧结扎诱导,动物通过浸入液氮处死。以氯胺酮作为全身麻醉剂进行双侧结扎导致磷脂酶A2活性迅速短暂增加。活性从结扎0分钟时的0.46 nmol/h/mg蛋白增加到结扎1分钟时的0.82 nmol/h/mg蛋白。磷脂酶A1活性在第1分钟内也从0.7增加到1.3 nmol/h/mg蛋白。当使用戊巴比妥作为麻醉剂时,磷脂酶激活更早,在最初30秒内。在未麻醉的情况下断头诱导Wistar大鼠缺血也发现了类似结果。已知沙土鼠双侧结扎颈动脉会增加游离脂肪酸的浓度,尤其是花生四烯酸。这种增加至少部分是由于磷脂酶A激活。由于脑中的乙醇胺磷脂酶A2活性不需要Ca2+,这些结果表明缺血脑中磷脂酶A2激活是由该酶的共价修饰引起的。