Mechanisms of mitochondrial calcium transport.
Mechanisms of mitochondrial calcium transport.
复制标题
线粒体钙转运机制。
DOI：
10.1007/978-1-4757-0007-7_1
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发表时间：
1988
影响因子：
--
通讯作者：
Gunter,KK
中科院分区：
文献类型：
--
作者：
Gunter,TE;Wingrove,DE;Banerjee,S;Gunter,KK
已知线粒体具有快速钙摄取机制或单端口以及钠依赖性和钠非依赖性流出机制。是否介导了不依赖于钠的钙流出以及是否可以在肝线粒体中发现钠依赖的钙流出已受到质疑。与这些问题的答案相关的动力学结果将在下面讨论。确定了一种缓慢的、介导的、不依赖于钠的钙流出机制，其显示出二级动力学。该机制显示出“非必要激活”动力学，其最大 Vmax 约为每毫克蛋白质每分钟 1.2 纳摩尔钙，最大速度的一半约为每毫克蛋白质 8.4 纳摩尔钙。确定了一种缓慢的、钠依赖性钙流出机制，该机制在钙中为一级，在钠中为二级。该机制的 Vmax 约为每分钟每毫克蛋白质 2.6 nmol 钙。钠依赖性在外部钠浓度为 9.4 mM 时半饱和，钙依赖性在内部钙浓度为每毫克蛋白质 8.1 nmol 钙时半饱和。钠依赖性的协同性有效地允许陆地反应物系统适合双反应物模型，其中[Na]仅以[Na]的平方出现。该肝脏系统表现出同步动力学，而不是乒乓动力学。人们还发现它对四苯基膦、镁和钌红的抑制很敏感。提出了一种模型，其中线粒体钙转运可以发挥作用以“塑造胞浆钙的脉冲”。同时，线粒体可能介导“钙记忆”，可能与通过钙调蛋白激活胞质事件有关，或者可能与通过线粒体内钙激活特定脱氢酶而激活电子传递有关。
Mitochondria are known to possess a rapid calcium uptake mechanism or uniport and both sodium-dependent and sodium-independent efflux mechanisms. Whether sodium-independent calcium efflux is mediated and whether sodium-dependent calcium efflux can be found in liver mitochondria have been questioned. Kinetics results relevant to the answers of these questions are discussed below.A slow, mediated, sodium-independent calcium efflux mechanism is identified which shows second order kinetics. This mechanism, which shows “nonessential activation” kinetics, has a Vmaxaround 1.2 nmol calcium per mg protein per min and a half maximal velocity around 8.4 nmol calcium per mg protein.A slow, sodium-dependent calcium efflux mechanism is identified, which is first order in calcium and second order in sodium. This mechanism has a Vmaxaround 2.6 nmol of calcium per mg protein per min. The sodium dependence is half saturated at an external sodium concentration of 9.4 mM, and the calcium dependence is half saturated at an internal calcium concentration of 8.1 nmol calcium per mg protein. The cooperativity of the sodium dependence effectively permits a terreactant system to be fit by a bireactant model in which [Na] only appears as the square of [Na]. This liver system shows simultaneous, as opposed to ping-pong, kinetics. It is also found to be sensitive to inhibition by tetraphenylphosphonium, magnesium, and ruthenium red.A model is proposed in which mitochondrial calcium transport could function to “shape the pulses” of cytosolic calcium. Simultaneously, mitochondria may mediate a “calcium memory” coupled perhaps to activation of cytosolic events through calmodulin or perhaps to activation of electron transport through the activation of specific dehydrogenases by intramitochondrial calcium.