ArticleThe Journal of biological chemistry2015
Sulfide oxidation by a noncanonical pathway in red blood cells generates thiosulfate and polysulfides.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 165 citations in OpenAlex.
- Molecular crosstalk between gas transmitters and catecholamine biosynthesis pathways: a narrative review.Medical gas research · 2027Review
- Self-bioRxiv : the preprint server for biology · 2026Article
- Physiological Roles of Hydrogen Sulfide/Polysulfides and Regulation of their Production.Handbook of experimental pharmacology · 2026Review
- Power and poison: The intersections of HThe Journal of biological chemistry · 2025Review
- Hydrogen sulfide in placental development and pregnancy disorders: mechanisms, therapeutic potential, and translational challenges.Reproductive biology and endocrinology : RB&E · 2025Review
- Gut sulfide metabolism modulates behavior and brain bioenergetics.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The therapeutic potential of hydrogen sulfide and its donors, a new discovery in vascular diseases.Journal of cardiovascular pharmacology · 2025Article
- Thiosulphate sulfurtransferase: Biological roles and therapeutic potential.Redox biology · 2025Review
- Essential role of sulfide oxidation in brain health and neurological disorders.Pharmacology & therapeutics · 2025Review
- Hydrogen sulfide as a new therapeutic target of pulmonary hypertension: an overview with update on immunomodulation.Frontiers in pharmacology · 2025Review
- Detoxification of hydrogen sulfide by synthetic heme model compounds.Scientific reports · 2024Article
- Emerging roles of hydrogen sulfide-metabolizing enzymes in cancer.Redox report : communications in free radical research · 2024Review
- Vitamin C-Dependent Uptake of Non-Heme Iron by Enterocytes, Its Impact on Erythropoiesis and Redox Capacity of Human Erythrocytes.Antioxidants (Basel, Switzerland) · 2024Review
- HAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Multimodal nanoimmunotherapy engages neutrophils to eliminate Staphylococcus aureus infections.Nature nanotechnology · 2024Article
- Exclusion of sulfide:quinone oxidoreductase from mitochondria causes Leigh-like disease in mice by impairing sulfide metabolism.The Journal of clinical investigation · 2024Article
- HProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Chemistry of Hydrogen Sulfide-Pathological and Physiological Functions in Mammalian Cells.Cells · 2023Review
- The Reactive Species Interactome in Red Blood Cells: Oxidants, Antioxidants, and Molecular Targets.Antioxidants (Basel, Switzerland) · 2023Article
- Emerging Chemical Biology of Protein Persulfidation.Antioxidants & redox signaling · 2023Review
23 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
A cardioprotectant at low concentrations, H2S is a toxin at high concentrations and inhibits cytochrome c oxidase. A conundrum in H2S homeostasis is its fate in red blood cells (RBCs), which produce H2S but lack the canonical mitochondrial sulfide oxidation pathway for its clearance. The sheer abundance of RBCs in circulation enhances the metabolic significance of their clearance strategy for H2S, necessary to avoid systemic toxicity. In this study, we demonstrate that H2S generation by RBCs is catalyzed by mercaptopyruvate sulfurtransferase. Furthermore, we have discovered the locus of sulfide oxidation in RBCs and describe a new role for an old protein, hemoglobin, which in the ferric or methemoglobin state binds H2S and oxidizes it to a mixture of thiosulfate and hydropolysulfides. Our study reveals a previously undescribed route for the biogenesis of hydropolysulfides, which are increasingly considered important for H2S-based signaling, but their origin in mammalian cells is unknown. An NADPH/flavoprotein oxidoreductase system restores polysulfide-carrying hemoglobin derivatives to ferrous hemoglobin, thus completing the methemoglobin-dependent sulfide oxidation cycle. Methemoglobin-dependent sulfide oxidation in mammals is complex and has similarities to chemistry reported for the dissolution of iron oxides in sulfidic waters and during bioleaching of metal sulfides. The catalytic oxidation of H2S by hemoglobin explains how RBCs maintain low steady-state H2S levels in circulation, and suggests that additional hemeproteins might be involved in sulfide homeostasis in other tissues.
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