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Positive feedback during sulfide oxidation fine-tunes cellular affinity for oxygen.
Abbas Abou-Hamdan1, Céline Ransy1, Thomas Roger2
1Inserm U1016, Institut Cochin, 75014 Paris, France; CNRS UM8104, Institut Cochin, 75014 Paris, France; Université Paris Descartes UMR-S1016, Institut Cochin, 75014 Paris, France.
Sulfide (H2S) influences cellular oxygen affinity by balancing its roles as an electron donor and cytochrome oxidase inhibitor. Its oxidation rate, not just concentration, dictates oxygen dependence in cells.
Area of Science:
- Biochemistry
- Cellular Respiration
- Mitochondrial Function
Background:
- Sulfide (H2S) is a gaseous transmitter impacting cellular respiration.
- H2S acts as both an electron donor and a potent inhibitor of cytochrome oxidase.
- The interplay between H2S oxidation and inhibition is critical for cellular oxygen utilization.
Purpose of the Study:
- To investigate how H2S release and oxidation affect cellular oxygen affinity.
- To elucidate the regulatory mechanisms of H2S in cellular respiration.
Main Methods:
- Cellular assays measuring H2S oxidation rates.
- Assessment of cellular dependence on oxygen under varying H2S conditions.
- Analysis of H2S concentrations in relation to metabolic rates.
Main Results:
- Cells exhibit heightened oxygen dependence as H2S delivery nears maximal oxidation rates.
- A positive feedback mechanism links H2S release and oxidation rates to oxygen affinity.
- Altered oxygen dependence is observable at low micromolar H2S concentrations.
Conclusions:
- Cellular H2S oxidation pathway activity modulates oxygen affinity during continuous H2S release.
- Reduced expression of the H2S oxidation pathway significantly increases cellular oxygen dependence.
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