Harrison 2015 J Appl Physiol
| Harrison DK, Fasching M, Fontana-Ayoub M, Gnaiger E (2015) Cytochrome redox states and respiratory control in mouse and beef heart mitochondria at steady-state levels of hypoxia. J Appl Physiol 119:1210-8. https://doi.org/10.1152/japplphysiol.00146.2015 |
Harrison David K, Fasching M, Fontana-Ayoub M, Gnaiger Erich (2015) J Appl Physiol
Abstract: Mitochondrial control of cellular redox states is a fundamental component of cell signaling in the coordination of core energy metabolism and homeostasis during normoxia and hypoxia. We investigated the relationship between cytochrome redox states and mitochondrial oxygen consumption at steady-state levels of hypoxia in mitochondria isolated from beef and mouse heart (BHimt, MHimt), comparing two species with different cardiac dynamics and local oxygen demands. A low-noise, rapid spectrophotometric system using visible light for the measurement of cytochrome redox states was combined with high-resolution respirometry. Monophasic hyperbolic relations were observed between oxygen consumption, JO2, and oxygen partial pressure, pO2, within the range <1.1 kPa (8.3 mmHg; 13 µM). p50j (pO2 at 0.5∙Jmax) was 0.015±0.0004 and 0.021±0.003 kPa (0.11 and 0.16 mmHg) for BHimt and MHimt, respectively. Maximum oxygen consumption, Jmax, was measured at saturating ADP levels (OXPHOS capacity) with Complex I-linked substrate supply. Redox states of cytochromes aa3 and c were biphasic hyperbolic functions of pO2. The relation between cytochrome oxidation state and oxygen consumption revealed a separation of distinct phases from mild to severe and deep hypoxia. When cytochrome c oxidation increased from fully reduced to 45 % oxidised at 0.1 Jmax, pO2 was as low as 0.002 kPa (0.02 µM), and trace amounts of oxygen are sufficient to partially oxidize the cytochromes. At higher pO2 under severe hypoxia, respiration increases steeply while redox changes are small. Under mild hypoxia, the steep slope of oxidation of cytochrome c when flux remains more stable represents a cushioning mechanism maintaining respiration high at the onset of hypoxia.
• Bioblast editor: Gnaiger E • O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck Oroboros
- This publication presents results obtained with a test prototype instrument of the O2k-Innovation.
MitoFit news 2015#14
- 2015-09-02: Defining mt-hypoxia at cytochrome redox steady-states with the O2k-Innovation. » MitoFit news
Cited by
- Gnaiger E (2024) Addressing the ambiguity crisis in bioenergetics and thermodynamics. MitoFit Preprints 2024.3. https://doi.org/10.26124/mitofit:2024-0003
- 9 articles in PubMed (2024-05-01) https://pubmed.ncbi.nlm.nih.gov/26251509/
Labels: MiParea: Respiration, Instruments;methods, Comparative MiP;environmental MiP
Stress:Hypoxia Organism: Mouse, Bovines Tissue;cell: Heart Preparation: Isolated mitochondria
Regulation: Oxygen kinetics, Redox state Coupling state: OXPHOS Pathway: N HRR: Oxygraph-2k, TIP2k, O2k-Spectrophotometer
MitoFitPublication, Steady state, Tissue normoxia, MitoFit2022Hypoxia, MitoFit2022rTCA, Gnaiger 2024 MitoFit
