Kapus A, Szászi K, Ligeti E
Department of Physiology, Semmelweis University Medical School, Budapest, Hungary.
Biochem J. 1992 Feb 1;281 ( Pt 3)(Pt 3):697-701. doi: 10.1042/bj2810697.
The mode of activation of an H(+)-conducting pathway present in the membrane of neutrophils was investigated. (1) Resting neutrophils released protons through an electrogenic Cd(2+)-inhibitable (K0.5 approximately 20 microM) route when a pH gradient and appropriate charge compensation was provided. (2) The rate of H+ efflux was stimulated over 2.5-fold by 4 beta-phorbol 12-myristate 13-acetate (PMA; K0.5 approximately 0.7 nM) or by 4 beta-phorbol 12,13-dibutyrate (K0.5 approximately 20 nM) even when the NADPH oxidase was blocked by p-chloromercuribenzoate. (3) Staurosporine inhibited the effect of PMA. (4) The H+ egress was not enhanced by 4 alpha-phorbol 12,13-didecanoate. (5) Low concentrations of Cd2+ (less than 40 microM) inhibited the H+ flux without influencing the oxidase. The results raise the possibility that protein kinase C could be involved in the activation of an electrogenic H(+)-conducting pathway in the membrane of neutrophils. The activation of this route by phorbol esters seems to be independent of the stimulation of NADPH oxidase.
研究了中性粒细胞膜中存在的H(+)传导途径的激活模式。(1) 当提供pH梯度和适当的电荷补偿时，静息中性粒细胞通过一种电致性的、Cd(2+)可抑制的（K0.5约为20 microM）途径释放质子。(2) 即使NADPH氧化酶被对氯汞苯甲酸阻断，4β-佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA；K0.5约为0.7 nM）或4β-佛波醇12,13-二丁酸酯（K0.5约为20 nM）也能将H+外流速率刺激超过2.5倍。(3) 星形孢菌素抑制PMA的作用。(4) 4α-佛波醇12,13-二癸酸酯不会增强H+外流。(5) 低浓度的Cd2+（小于4 microM）抑制H+通量而不影响氧化酶。这些结果增加了蛋白激酶C可能参与中性粒细胞膜中电致性H(+)传导途径激活的可能性。佛波酯对该途径的激活似乎独立于NADPH氧化酶的刺激。
