Markert M, Vaglio M, Frei J
Central Laboratory of Clinical Chemistry, CHUV, Lausanne, Switzerland.
J Lab Clin Med. 1988 May;111(5):577-83.
We found that 4,4'-diisothiocyano-2,2'-disulfonic acid (DIDS), an anion channel blocker in erythrocytes, caused a concentration-related stimulation of oxygen radicals in human neutrophils, as measured by luminol- and lucigenin-amplified chemiluminescence. The DIDS-elicited oxygen radical burst followed the kinetic pattern of other stimuli with a lag period of 20 seconds, reaching a maximum after 12 to 15 minutes. Washing neutrophils that had been pretreated with DIDS did not reverse neutrophil activation. DIDS was found to strongly stimulate lactate production and did not block the efflux of this anion. Cytochalasin B completely abolished the chemiluminescence responses when added before DIDS stimulation. It also inhibited lactate production, however, only in a glucose-containing medium. Modulation of oxygen radical production by DIDS may reveal an additional transductional pathway for neutrophil activation.
我们发现，红细胞阴离子通道阻滞剂4,4'-二异硫氰基-2,2'-二磺酸（DIDS）可引起人中性粒细胞中氧自由基浓度相关的刺激，这是通过鲁米诺和光泽精增强的化学发光法测量的。DIDS引发的氧自由基爆发遵循其他刺激的动力学模式，有20秒的延迟期，在12至15分钟后达到最大值。洗涤用DIDS预处理过的中性粒细胞并不能逆转中性粒细胞的活化。发现DIDS强烈刺激乳酸生成，并且不阻断该阴离子的外流。在DIDS刺激前加入细胞松弛素B可完全消除化学发光反应。它也抑制乳酸生成，然而，仅在含葡萄糖的培养基中。DIDS对氧自由基产生的调节可能揭示了中性粒细胞活化的另一种转导途径。
