A Case for Hydrogen Sulfide Metabolism as an Oxygen Sensing Mechanism

Olson, Kenneth R.

doi:10.3390/antiox10111650

Cited by 25 publications

(15 citation statements)

References 263 publications

(344 reference statements)

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“…The number of possible consequences caused by disturbances in cellular bioenergetics appears immense. However, in the first instance, the effects of sulfide donors, as well as mechanisms for oxygen sensing [44,[48][49][50], may benefit from consideration of these interferences that take place even if variations in the fluxes of these critical substrates remain of marginal quantitative importance.…”

Section: Discussionmentioning

confidence: 99%

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

Bouillaud

2022

Biomolecules

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The present article will not attempt to deal with sulfide per se as a signaling molecule but will aim to examine the consequences of sulfide oxidation by mitochondrial sulfide quinone reductase in mammalian cells. This oxidation appears first as a priority to avoid self-poisoning by endogenous sulfide and second to occur with the lowest ATP/O2 ratio when compared to other mitochondrial substrates. This is explained by the injection of electrons in the respiratory chain after complex I (as for succinate) and by a sulfur oxidation step implying a dioxygenase that consumes oxygen but does not contribute to mitochondrial bioenergetics. Both contribute to increase cellular oxygen consumption if sulfide is provided below its toxic level (low µM). Accordingly, if oxygen supply or respiratory chain activity becomes a limiting factor, small variations in sulfide release impact the cellular ATP/ADP ratio, a major metabolic sensor.

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Section: Discussionmentioning

confidence: 99%

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

Bouillaud

2022

Biomolecules

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“…Here, we only briefly describe basic concepts of RSS chemistry, which is rather complex. For more detailed information, we refer the reader to recent comprehensive reviews on this topic [ 14 , 15 ] (and references therein).…”

Section: Cellular Reactive Species Generationmentioning

confidence: 99%

Understanding Cellular Redox Homeostasis: A Challenge for Precision Medicine

Tretter

Hochreiter

Zach

et al. 2021

IJMS

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Living organisms use a large repertoire of anabolic and catabolic reactions to maintain their physiological body functions, many of which include oxidation and reduction of substrates. The scientific field of redox biology tries to understand how redox homeostasis is regulated and maintained and which mechanisms are derailed in diverse pathological developments of diseases, where oxidative or reductive stress is an issue. The term “oxidative stress” is defined as an imbalance between the generation of oxidants and the local antioxidative defense. Key mediators of oxidative stress are reactive species derived from oxygen, nitrogen, and sulfur that are signal factors at physiological concentrations but can damage cellular macromolecules when they accumulate. However, therapeutical targeting of oxidative stress in disease has proven more difficult than previously expected. Major reasons for this are the very delicate cellular redox systems that differ in the subcellular compartments with regard to their concentrations and depending on the physiological or pathological status of cells and organelles (i.e., circadian rhythm, cell cycle, metabolic need, disease stadium). As reactive species are used as signaling molecules, non-targeted broad-spectrum antioxidants in many cases will fail their therapeutic aim. Precision medicine is called to remedy the situation.

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“…The oxygen tension (PO 2 ), energy metabolism and blood flow vary among kidney regions. For instance, H 2 S oxidation in the mitochondria represents an alternative source for the synthesis of ATP (see Section 3.4), which is dependent on the PO 2 [192]. The PO 2 is higher in the renal cortex than in renal medulla [134,[193][194][195][196].…”

Section: Cysteine Contribution For Kidney Adaptation To Hypoxiamentioning

confidence: 99%

Cysteine as a Multifaceted Player in Kidney, the Cysteine-Related Thiolome and Its Implications for Precision Medicine

et al. 2022

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In this review encouraged by original data, we first provided in vivo evidence that the kidney, comparative to the liver or brain, is an organ particularly rich in cysteine. In the kidney, the total availability of cysteine was higher in cortex tissue than in the medulla and distributed in free reduced, free oxidized and protein-bound fractions (in descending order). Next, we provided a comprehensive integrated review on the evidence that supports the reliance on cysteine of the kidney beyond cysteine antioxidant properties, highlighting the relevance of cysteine and its renal metabolism in the control of cysteine excess in the body as a pivotal source of metabolites to kidney biomass and bioenergetics and a promoter of adaptive responses to stressors. This view might translate into novel perspectives on the mechanisms of kidney function and blood pressure regulation and on clinical implications of the cysteine-related thiolome as a tool in precision medicine.

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A Case for Hydrogen Sulfide Metabolism as an Oxygen Sensing Mechanism

Cited by 25 publications

References 263 publications

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

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

Understanding Cellular Redox Homeostasis: A Challenge for Precision Medicine

Cysteine as a Multifaceted Player in Kidney, the Cysteine-Related Thiolome and Its Implications for Precision Medicine

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