Féray J C, Guerrouache K, Garay R P
School of Medicine, INSERM U400, 8 rue du Général Sarrail, Créteil Cédex, 94010, France.
Biochem Biophys Res Commun. 2000 Feb 24;268(3):673-6. doi: 10.1006/bbrc.2000.2195.
When incubated in 150 mM KCl, rat thymocytes exhibited a very important magnesium efflux (11.4 +/- 0.7 mmoles/liter cells/20 min, n = 29), about 90 times higher than the physiological magnesium efflux catalyzed by the Na-Mg exchanger (0.126 +/- 0.093 mmoles/liter cells/20 min). Cells remained viable (trypan blue test) and membrane integrity was shown by the absence of an increase in sodium permeability. K(+)-induced magnesium efflux exhibited the following properties: (i) it required the presence of external chloride; (ii) it was fully blocked by DIOA, a selective KCl-cotransporter inhibitor (IC(50) = 35 microm); and (iii) it was associated to a progressive increase in cell volume via the DIOA-sensitive K-Cl cotransporter. Such cell swelling seems to play a causal role, because (i) hypertonic media (+400 mM sucrose) abolished K(+)-induced magnesium efflux and (ii) hypotonic Ringer media (205 mOsm) increased both cell volume and magnesium efflux (from a basal value of 0.35 +/- 0.03 mmoles/liter cells/20 min up to 1.44 +/- 0.24 mmoles/liter cells/20 min), even in the presence of DIOA. In conclusion, high potassium induced a dramatic release of intracellular magnesium from rat thymocytes. Such a phenomenon was, at least in part, caused by cell swelling via the DIOA-sensitive K-Cl cotransporter. The nature of the magnesium transport mechanism and its role in the transduction signal of K-Cl cotransporter activation by cell swelling deserve further investigation.
当在150 mM KCl中孵育时，大鼠胸腺细胞表现出非常显著的镁外流（11.4±0.7毫摩尔/升细胞/20分钟，n = 29），比钠-镁交换体催化的生理性镁外流（0.126±0.093毫摩尔/升细胞/20分钟）高约90倍。细胞保持存活（台盼蓝试验），并且通过钠通透性未增加表明膜完整性良好。钾诱导的镁外流具有以下特性：（i）它需要细胞外氯离子的存在；（ii）它被DIOA（一种选择性KCl共转运体抑制剂，IC50 = 35微摩尔）完全阻断；（iii）它通过对DIOA敏感的K-Cl共转运体与细胞体积的逐渐增加相关。这种细胞肿胀似乎起因果作用，因为（i）高渗培养基（+400 mM蔗糖）消除了钾诱导的镁外流，并且（ii）低渗林格氏培养基（205 mOsm）即使在存在DIOA的情况下也增加了细胞体积和镁外流（从基础值0.35±0.03毫摩尔/升细胞/20分钟增加到1.44±0.24毫摩尔/升细胞/20分钟）。总之，高钾诱导大鼠胸腺细胞内镁的大量释放。这种现象至少部分是由通过对DIOA敏感的K-Cl共转运体引起的细胞肿胀所致。镁转运机制的性质及其在细胞肿胀激活K-Cl共转运体的转导信号中的作用值得进一步研究。
