Dieter P
Biochemisches Institut, Albert-Ludwigs-Universität, Freiburg, Germany.
FEBS Lett. 1992 Feb 17;298(1):17-20. doi: 10.1016/0014-5793(92)80012-6.
Activation of the superoxide-generating NADPH oxidase by phorbol ester or zymosan induced a cytoplasmic acidification when liver macrophages were incubated in sodium-free media or in the presence of amiloride. Staurosporine or desensitization of protein kinase C inhibited phorbol ester- and zymosan-induced pH changes and generation of superoxide. The intracellular pH remained unchanged in cells incubated in physiological sodium media. Ionomycin and arachidonic acid did not induce a change in intracellular pH or a generation of superoxide. Fluoride, which has been shown to induce a translocation of protein kinase C in these cells, did not elicit superoxide generation but induced a decrease in intracellular pH. These experiments support (1) a role of the Na+/H+ antiporter in macrophages as a metabolic regulator of intracellular pH upon stimulation of the superoxide-generating NADPH oxidase, and (2) suggest an involvement of protein kinase C in this process.
当肝巨噬细胞在无钠培养基中或存在氨氯吡脒的情况下孵育时，佛波酯或酵母聚糖激活产生超氧化物的NADPH氧化酶会导致细胞质酸化。星形孢菌素或蛋白激酶C脱敏可抑制佛波酯和酵母聚糖诱导的pH变化以及超氧化物的产生。在生理钠培养基中孵育的细胞内pH保持不变。离子霉素和花生四烯酸不会引起细胞内pH变化或超氧化物的产生。氟化物已被证明可诱导这些细胞中蛋白激酶C的转位，它不会引发超氧化物的产生，但会导致细胞内pH降低。这些实验支持：（1）Na+/H+反向转运蛋白在巨噬细胞中作为刺激产生超氧化物的NADPH氧化酶时细胞内pH的代谢调节剂的作用；（2）提示蛋白激酶C参与了这一过程。
