Jones G S, VanDyke K, Castranova V
J Cell Physiol. 1981 Jan;106(1):75-83. doi: 10.1002/jcp.1041060109.
Treatment of human granulocytes with concanavalin A, phorbol myristate acetate (PMA), N-formyl-methionyl-leucyl-phenylalanine (FMLP), and A23187 (a calcium ionophore) stimulates the release of superoxide anion and the generation of chemiluminescence. The fluorescent probe, Di-S-C3(5), has been used to monitor shifts in membrane potential in response to these stimulants which precede the secretion of superoxide. Concanavalin A, PMA, and FMLP induce a biphasic shift in transmembrane potential (Em), i.e., a rapid depolarization followed by a prolonged hyperpolarization. This depolarization is dependent on both external sodium and calcium while the hyperpolarization is inhibited by ouabain which blocks the electrogenic Na-K pump. In contrast, A23187 induces a rapid and prolonged depolarization. This monophasic shift in Em is dependent on external calcium. These results suggest that depolarization acts as a signal to initiate events associated with the "respiratory burst" of these phagocytes.
用刀豆球蛋白A、佛波酯（PMA）、N-甲酰甲硫氨酰亮氨酰苯丙氨酸（FMLP）和A23187（一种钙离子载体）处理人粒细胞，可刺激超氧阴离子的释放和化学发光的产生。荧光探针Di-S-C3(5)已被用于监测这些刺激剂作用下膜电位的变化，这些变化先于超氧阴离子的分泌。刀豆球蛋白A、PMA和FMLP会引起跨膜电位（Em）的双相变化，即快速去极化，随后是长时间的超极化。这种去极化依赖于细胞外的钠和钙，而超极化则被抑制钠钾泵的哇巴因所抑制。相比之下，A23187会引起快速且持续的去极化。这种Em的单相变化依赖于细胞外钙。这些结果表明，去极化作为一种信号启动与这些吞噬细胞“呼吸爆发”相关的事件。
