Pyridine nucleotide as an indicator of the oxygen requirements for energy-linked functions of mitochondria.
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.
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D002118:Calcium / Q000378:metabolism; D003574:Cytochrome c Group / Q000378:metabolism; D004579:Electron Transport; D000860:Hypoxia / Q000378:metabolism; D008564:Membrane Potentials; D008931:Mitochondria, Muscle / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D009243:NAD; D010084:Oxidation-Reduction; D010101:Oxygen Consumption
D003574:Cytochrome c Group; D009243:NAD; D000255:Adenosine Triphosphate; D002118:Calcium