Hansford R G
Laboratory of Cardiovascular Science, National Institute on Aging, Baltimore, Maryland 21224.
J Bioenerg Biomembr. 1991 Dec;23(6):823-54. doi: 10.1007/BF00786004.
The activation of intramitochondrial dehydrogenases by Ca2+ provides a link between the intensity of work performance by a tissue and the activity of pyruvate dehydrogenase and the tricarboxylate cycle, and hence the rate of ATP production by the mitochondria. Several aspects of this model of the control of oxidative phosphorylation are examined in this article, with particular emphasis on mitochondrial functioning in situ in cardiac myocytes and in the intact heart. Recent use of the fluorescent Ca2+ chelating agents indo-1 and fura-2 has allowed a more quantitative description of the dependence of dehydrogenase activity upon concentration of free intramitochondrial Ca2+, in experiments with isolated mitochondria. Further, a novel technique developed by Miyata et al. has allowed description of free intramitochondrial Ca2+ within a single cardiac myocyte, and the conclusion that this parameter changes in response to electrical excitation of the cell over a range which would be expected to give substantial modulation of dehydrogenase activity.
钙离子对线粒体内脱氢酶的激活作用，在组织的工作强度与丙酮酸脱氢酶活性及三羧酸循环之间建立了联系，进而与线粒体的ATP生成速率相关。本文探讨了这种氧化磷酸化调控模型的几个方面，特别强调了心肌细胞和完整心脏中线粒体的原位功能。最近，荧光钙离子螯合剂indo-1和fura-2在分离线粒体的实验中，使人们能够更定量地描述脱氢酶活性对线粒体内游离钙离子浓度的依赖性。此外，宫田等人开发的一项新技术，能够描述单个心肌细胞内的线粒体内游离钙离子，并且得出结论：该参数会随着细胞的电兴奋在一定范围内发生变化，而这个范围预计会对脱氢酶活性产生显著调节作用。
