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Sulfide Oxidation Evidences the Immediate Cellular Response to a Decrease in the Mitochondrial ATP/O2 Ratio.

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Biomolecules
|March 25, 2022
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Sulfide oxidation by mitochondrial sulfide quinone reductase prevents cell poisoning and consumes oxygen. This process impacts cellular energy levels, particularly the ATP/ADP ratio, when oxygen or respiratory activity is limited.

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Area of Science:

  • Cellular biochemistry
  • Mitochondrial function
  • Metabolic regulation

Background:

  • Sulfide (H2S) is endogenously produced and can be toxic at high concentrations.
  • Mitochondria play a crucial role in cellular energy production and detoxification.
  • Mitochondrial sulfide quinone reductase (SQR) is involved in sulfide metabolism.

Purpose of the Study:

  • To investigate the consequences of sulfide oxidation by SQR in mammalian cells.
  • To understand the bioenergetic implications of sulfide oxidation.
  • To explore the role of sulfide oxidation in cellular oxygen consumption and ATP production.

Main Methods:

  • Focus on the biochemical consequences of sulfide oxidation by SQR.
  • Analysis of electron injection into the respiratory chain.
  • Assessment of oxygen consumption and ATP/O2 ratios.
  • Evaluation of cellular ATP/ADP ratio under varying sulfide levels.

Main Results:

  • Sulfide oxidation by SQR prioritizes detoxification over ATP production.
  • Sulfide oxidation occurs with a low ATP/O2 ratio due to electron injection post-Complex I and oxygen-consuming sulfur oxidation.
  • Cellular oxygen consumption increases with low micromolar sulfide levels.
  • Sulfide release variations significantly impact the ATP/ADP ratio when oxygen or respiratory chain activity is limited.

Conclusions:

  • Sulfide oxidation by SQR is a critical protective mechanism against endogenous sulfide toxicity.
  • The bioenergetic cost of sulfide oxidation influences cellular energy homeostasis.
  • The ATP/ADP ratio serves as a sensitive metabolic sensor to sulfide fluctuations under limiting respiratory conditions.