Chernyak B V
Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, 119899, Russia.
Biochemistry (Mosc). 1999 Aug;64(8):922-8.
Increase of Ca2+ concentration in the cytosol of thymocytes to 400-600 nM causes slow accumulation of Ca2+ in mitochondria. Release of Ca2+ from mitochondria into the cytosol is induced by an uncoupler (FCCP) or by a dithiol cross-linking agent (phenylarsine oxide) and is inhibited by cyclosporin A--a specific inhibitor of the permeability transition pore in the inner mitochondrial membrane. In the presence of oxidizing agents (tert-butyl hydroperoxide and diamide), sub-optimal concentrations of uncoupler induce rapid cyclosporin-sensitive release of Ca2+. 6-Ketocholestanol, a recoupler under these conditions, causes redistribution of Ca2+ from the cytosol into mitochondria. These data indicate that partial uncoupling under conditions of oxidative stress causes opening of the permeability transition pore in a fraction of the mitochondria in intact lymphocytes. This mechanism mediates rapid release of Ca2+ from mitochondria into the cytosol.
胸腺细胞胞质溶胶中Ca2+浓度升高至400 - 600 nM会导致Ca2+在线粒体中缓慢积累。线粒体中的Ca2+释放到胞质溶胶是由解偶联剂（FCCP）或二硫醇交联剂（苯砷氧化物）诱导的，并受到环孢素A的抑制，环孢素A是线粒体内膜通透性转换孔的特异性抑制剂。在氧化剂（叔丁基过氧化氢和二酰胺）存在的情况下，次优浓度的解偶联剂会诱导环孢素敏感的Ca2+快速释放。6 - 酮胆甾醇在这些条件下是一种再偶联剂，会导致Ca2+从胞质溶胶重新分布到线粒体中。这些数据表明，氧化应激条件下的部分解偶联会导致完整淋巴细胞中一部分线粒体的通透性转换孔开放。这种机制介导了Ca2+从线粒体快速释放到胞质溶胶中。
