Walsh C E, Dechatelet L R, Thomas M J, O'Flaherty J T, Waite M
Lipids. 1981 Feb;16(2):120-4. doi: 10.1007/BF02535685.
Challenge of human neutrophils prelabeled with [3H] arachidonate and [14C] palmitate or [14C]-stearate with opsonized zymosan or the Ca2+ ionophores A23187 or Ionomycin caused the release of [3H], but not [14C], fatty acid. With the ionophores, but not zymosan, considerable conversion of the [3H] arachidonate to hydroxyeicosatetraenoates occurred. Although various isomers were recovered, the 5-hydroxyeicosatetraenoate appeared to be the major product. In these experiments, no [14C] products were detected such as lysophospholipid, diglyceride or monoglyceride. Although no definite statement can be made about the mechanism of release of arachidonate, our data are most easily interpreted as the result of the action of a phospholipase A2.
用[3H]花生四烯酸和[14C]棕榈酸或[14C]硬脂酸预标记的人中性粒细胞，与调理酵母聚糖或Ca2+离子载体A23187或离子霉素发生反应，导致[3H]脂肪酸释放，但[14C]脂肪酸未释放。使用离子载体时，而非酵母聚糖，[3H]花生四烯酸会大量转化为羟基二十碳四烯酸。尽管回收了各种异构体，但5-羟基二十碳四烯酸似乎是主要产物。在这些实验中，未检测到[14C]产物，如溶血磷脂、甘油二酯或甘油单酯。尽管关于花生四烯酸释放机制无法给出确切说明，但我们的数据最容易解释为磷脂酶A2作用的结果。
