Dorio R J, Nelson J, Forman H J
Biochim Biophys Acta. 1987 Apr 22;928(2):137-43. doi: 10.1016/0167-4889(87)90114-5.
Superoxide production in alveolar macrophages is stimulated by agonists which act through Ca2+-mediated (concanavalin A) and/or protein kinase C (phorbol ester or diacylglycerol analogues) -mediated events. Simultaneous addition of saturating concentrations of concanavalin A and a protein kinase C activator (either phorbol 12-myristate-13-acetate or 1-oleoyl-2-acetyl-sn-glycerol) caused a supra-additive enhancement of the initial rate of O2-. production. This synergism closely correlated with the known time-course of Ca2+ mobilization induced by concanavalin A; however, it occurred under conditions in which protein kinase C activation is reportedly not Ca2+ dependent. Phorbol ester-induced O2-. production was partially inhibited by the Ca2+ ionophore, A23187. Although phorbol ester-stimulated O2-. production initially was enhanced by concanavalin A, the duration of this O2-. production was reduced in comparison to that induced by phorbol ester alone. These results suggest a dual role for intracellular Ca2+ in both stimulatory and inhibitory regulation of O2-. production.
通过Ca2 +介导（伴刀豆球蛋白A）和/或蛋白激酶C（佛波酯或二酰基甘油类似物）介导的事件起作用的激动剂可刺激肺泡巨噬细胞中超氧化物的产生。同时加入饱和浓度的伴刀豆球蛋白A和蛋白激酶C激活剂（佛波酯12 - 肉豆蔻酸酯 - 13 - 乙酸酯或1 - 油酰基 - 2 - 乙酰 - sn - 甘油）可导致O2 -产生初始速率的超加成增强。这种协同作用与伴刀豆球蛋白A诱导的Ca2 +动员的已知时间进程密切相关；然而，它发生在据报道蛋白激酶C激活不依赖Ca2 +的条件下。佛波酯诱导的O2 -产生被Ca2 +离子载体A23187部分抑制。尽管伴刀豆球蛋白A最初增强了佛波酯刺激的O2 -产生，但与单独由佛波酯诱导的相比，这种O2 -产生的持续时间缩短了。这些结果表明细胞内Ca2 +在O2 -产生的刺激和抑制调节中具有双重作用。
