Dransfield D T, Aprille J R
Department of Biology, Tufts University, Medford, Massachusetts 02155.
Am J Physiol. 1993 Mar;264(3 Pt 1):C663-70. doi: 10.1152/ajpcell.1993.264.3.C663.
This study investigated the cellular regulation of net adenine nucleotide movements between the cytoplasm and mitochondria in intact cells. Such movements are presumed to occur primarily by ATP-Mg exchange with Pi via the mitochondrial ATP-Mg/Pi carrier. Vasopressin, A23187, and thapsigargin all elevate intracellular free [Ca2+] and all caused dose-dependent increases in the mitochondrial adenine nucleotide content (29, 63, and 39%, respectively). Phorbol 12-myristate 13-acetate had no effect. The effect of vasopressin was abolished when cytoplasmic [ATP] was decreased (by 43%) and [Pi] was increased (3-fold) by addition of carboxyatractyloside. The effect of thapsigargin was abolished by addition of xylulose to deplete cytoplasmic [ATP] (by 50%) and [Pi] (> 4-fold). The results indicate that in intact cells Ca2+ activates the mitochondrial ATP-Mg/Pi carrier to enable changes in the subcellular distribution of adenine nucleotides and that the relative [ATP] and [Pi] gradients govern the direction and magnitude of net adenine nucleotide movements between the cytoplasm and mitochondria.
本研究调查了完整细胞中腺嘌呤核苷酸在细胞质和线粒体之间净移动的细胞调节机制。这种移动据推测主要通过线粒体ATP-Mg/Pi载体与Pi进行ATP-Mg交换而发生。血管加压素、A23187和毒胡萝卜素均可提高细胞内游离[Ca2+]浓度，且均导致线粒体腺嘌呤核苷酸含量呈剂量依赖性增加（分别为29%、63%和39%）。佛波酯12-肉豆蔻酸酯13-乙酸酯无此作用。加入羧基苍术苷使细胞质[ATP]降低（43%）且[Pi]升高（3倍）后，血管加压素的作用消失。加入木酮糖以耗尽细胞质[ATP]（50%）和[Pi]（>4倍）后，毒胡萝卜素的作用消失。结果表明，在完整细胞中，Ca2+激活线粒体ATP-Mg/Pi载体，使腺嘌呤核苷酸的亚细胞分布发生变化，且相对[ATP]和[Pi]梯度决定了腺嘌呤核苷酸在细胞质和线粒体之间净移动的方向和幅度。
