Riley W W, Pfeiffer D R
J Biol Chem. 1986 Jan 5;261(1):28-31.
A novel mitochondrial Ca2+ release phenomenon is reported. When rat liver mitochondria (oxidizing succinate) are allowed to accumulate Ca2+ in excess of 40 nmol/mg protein and are then treated with excess EGTA, a fraction of the accumulated cation is rapidly (approximately 1 nmol/s/mg protein) released. The size of the released fraction is an apparent function of the extramitochondrial Ca2+ concentration at the time of EGTA addition and can attain a maximal value of approximately 30 nmol/mg protein. Release is inhibited by ruthenium red (I50 approximately 50 pmol/mg protein) and is not dependent on the presence of Na+ or K+ in the medium. During the period of rapid release, O2 consumption is inhibited, membrane potential increases, and apparent H+ accumulation occurs at a ratio of approximately 2H+ per Ca2+ released. It is proposed that this chelator-induced Ca2+ release occurs by reverse uniport with H+ back diffusion to the matrix space providing charge movement compensation.
据报道，一种新的线粒体Ca2+释放现象。当大鼠肝脏线粒体（氧化琥珀酸）积累的Ca2+超过40 nmol/mg蛋白质，然后用过量的乙二醇双（2-氨基乙基醚）四乙酸（EGTA）处理时，一部分积累的阳离子会迅速（约1 nmol/s/mg蛋白质）释放。释放部分的大小显然是添加EGTA时线粒体外Ca2+浓度的函数，并且可以达到约30 nmol/mg蛋白质的最大值。释放受到钌红抑制（半数抑制浓度约为50 pmol/mg蛋白质），且不依赖于培养基中Na+或K+的存在。在快速释放期间，氧气消耗受到抑制，膜电位增加，并且以每释放1个Ca2+约2个H+的比例出现明显的H+积累。有人提出，这种螯合剂诱导的Ca2+释放是通过反向单向运输发生的，H+反向扩散到基质空间以提供电荷移动补偿。
