Gáspár R, Bene L, Damjanovich S, Muñoz-Garay C, Calderon-Aranda E S, Possani L D
Department of Biophysics, University Medical School, Debrecen, Hungary.
Biochem Biophys Res Commun. 1995 Aug 15;213(2):419-23. doi: 10.1006/bbrc.1995.2148.
Using the patch-clamp technique, we determined that beta-scorpion toxin 2 from Centruroides noxius Hoffmann decreased whole-cell n-type K+ currents in human peripheral blood lymphocytes, with a half blocking concentration of approx. 5 microM. Toxin-2-accelerated inactivation, however, did not influence the kinetics of activation of the K+ conductance. The percentage increase in K+ channel inactivation rate and the degree of drug-induced block was independent of membrane potential. K+ channel block by Toxin 2 was instantaneous, not removable by washing with drug free extracellular solution. However, 10 mg/ml BSA in the bath lifted the toxin-induced block almost instantaneously and completely. Flow cytometric membrane potential measurements with the oxonol dye showed that Toxin 2 depolarizes human lymphocytes in concert with its K+ channel blocking effect.
运用膜片钳技术,我们确定了来自墨西哥毒蝎(Centruroides noxius Hoffmann)的β-蝎毒素2可降低人外周血淋巴细胞中的全细胞N型钾电流,其半数阻断浓度约为5微摩尔。然而,毒素2加速的失活并未影响钾电导的激活动力学。钾通道失活速率的增加百分比和药物诱导的阻断程度与膜电位无关。毒素2对钾通道的阻断是瞬时的,用无药物的细胞外溶液冲洗无法消除。然而,浴槽中10毫克/毫升的牛血清白蛋白几乎能立即且完全解除毒素诱导的阻断。用羰花青染料进行的流式细胞仪膜电位测量表明,毒素2在阻断钾通道的同时会使人类淋巴细胞去极化。