Spät András, Pitter János G
Laboratory of Cellular and Molecular Physiology and Department of Physiology, Semmelweis University, Faculty of Medicine, P.O. Box 259, H-1444 Budapest, Hungary.
Mol Cell Endocrinol. 2004 Feb 27;215(1-2):115-8. doi: 10.1016/j.mce.2003.11.004.
As first observed in rat adrenal glomerulosa cells, cytoplasmic Ca(2+) signal, induced by K(+), angiotensin II or vasopressin, evokes an increase in the level of reduced mitochondrial pyridine nucleotides, NADH and NADPH. Prostaglandin F(2)alpha and extracellular ATP exert similar effects in rat ovarian luteal cells. This coupling of cytoplasmic Ca(2+) concentration and mitochondrial metabolism occurs also when the stimuli are applied at physiological concentration and under conditions when no formation of high-Ca(2+) perimitochondrial microdomains may be presumed. We present evidence that low submicromolar Ca(2+) signals in the cytoplasm can increase mitochondrial Ca(2+) concentration and activate mitochondrial dehydrogenation processes. Several observations support the assumption that intramitochondrial Ca(2+) signals play a significant role in the stimulation of steroid hormone production.
正如在大鼠肾上腺球状带细胞中首次观察到的那样，由钾离子、血管紧张素II或血管加压素诱导的细胞质钙离子信号，会引发线粒体中还原型吡啶核苷酸、NADH和NADPH水平的升高。前列腺素F2α和细胞外ATP在大鼠卵巢黄体细胞中发挥类似作用。当在生理浓度下施加刺激且假定不会形成高钙离子浓度的线粒体外周微区的条件下，细胞质钙离子浓度与线粒体代谢之间的这种偶联也会发生。我们提供的证据表明，细胞质中低亚微摩尔浓度的钙离子信号可增加线粒体钙离子浓度并激活线粒体脱氢过程。多项观察结果支持线粒体内钙离子信号在刺激类固醇激素产生中起重要作用这一假设。
