Höser N, Dawczynski H, Winnefeld K, Dargel R
Acta Biol Med Ger. 1978;37(1):19-29.
Inorganic phosphate stimulates the release of Mg++ from liver mitochondria, depending on concentration; a concentration as low as 0.1 mM phosphate is already effective. The process is dependent on the electron transfer of the respiratory chain, and its rate is highest under conditions of endogenous respiration and with ascorbate and TMPD as substrates, respectively. The phosphate stimulated release of Mg++ is followed, with a pronounced delay, by a Ca++ efflux and a swelling of mitochondria. Addition of EGTA strongly reduced the rate of Mg++ liberation in the presence and absence of inorganic phosphate. Exogenous Ca++ is able to abolish the EGTA effect. ADP and ATP inhibit the phosphate stimulated release of Mg++. Phosphoenol pyruvate and free fatty acids enhance the rate of Mg++ and Ca++ efflux from the mitochondria. The results permit the conclusion that inorganic phosphate, Ca++ and various metabolites of the cell metabolism influence the Mg++ distribution between the extra- and intramitochondrial space, thus controlling the permeability of the mitochondrial inner membrane for monovalent cations.
无机磷酸盐会刺激肝脏线粒体释放Mg++，这取决于其浓度；低至0.1 mM的磷酸盐浓度就已经有效。该过程依赖于呼吸链的电子传递，在内源呼吸条件下以及分别以抗坏血酸和TMPD作为底物时，其速率最高。磷酸盐刺激Mg++释放之后，会有明显延迟地接着出现Ca++外流和线粒体肿胀。添加EGTA会在有无无机磷酸盐的情况下都强烈降低Mg++释放的速率。外源Ca++能够消除EGTA的作用。ADP和ATP会抑制磷酸盐刺激的Mg++释放。磷酸烯醇丙酮酸和游离脂肪酸会提高Mg++和Ca++从线粒体流出的速率。这些结果可以得出结论，无机磷酸盐、Ca++以及细胞代谢的各种代谢产物会影响线粒体外和线粒体内空间之间的Mg++分布，从而控制线粒体内膜对单价阳离子的通透性。
