Chance B
Circ Res. 1976 May;38(5 Suppl 1):I31-8.
The responses of cardiac mitochondria to anoxia may be evaluated in terms of the oxidation-reduction state of the electron carriers and the ability of the mitochondria to function in energy-linked reactions. The previous detailed evaluation of the oxygen requirements for electron transfer in mitochondria is here extended to the oxygen requirements for energy-linked functions. Four functions are evaluated: the energy-dependent reduction of pyridine nucleotide, the phosphorylation of ADP, the retention of Ca2+, and the establishment of a membrane potential. All of these functions are half-maximally activated with 10-20% oxidation of cytochromes c and a + a3. Fifty percent oxidation of pyridine nucleotide is required for these functions. In a normoxic-anoxic titration, an increment of 50% in the reduction of pyridine nucleotide in intact tissue corresponds to the point at which the mitochondria are half-maximally active in energy coupling. Thus, the use of pyridine nucleotide fluorescence as an optimal indicator of tissue oxidation-reduction states has now been extended to the assay of energy-linked functions of mitochondria in situ in cardiac tissue.
心脏线粒体对缺氧的反应可以根据电子载体的氧化还原状态以及线粒体在能量偶联反应中发挥功能的能力来评估。先前对线粒体中电子传递所需氧气的详细评估在此扩展到能量偶联功能所需的氧气。评估了四种功能：吡啶核苷酸的能量依赖性还原、ADP的磷酸化、Ca2+的保留以及膜电位的建立。所有这些功能在细胞色素c和a + a3氧化10 - 20%时被激活到最大活性的一半。这些功能需要吡啶核苷酸氧化50%。在常氧-缺氧滴定中，完整组织中吡啶核苷酸还原增加50%对应于线粒体在能量偶联中活性达到最大活性一半的点。因此，吡啶核苷酸荧光作为组织氧化还原状态的最佳指标的应用现已扩展到心脏组织中线粒体原位能量偶联功能的测定。
