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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.[1]References
- Pyridine nucleotide as an indicator of the oxygen requirements for energy-linked functions of mitochondria. Chance, B. Circ. Res. (1976) [Pubmed]
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