Effect of hydrogen sulfide on glycolysis‐based energy production in mouse erythrocytes
| Autor: | Guangdong Yang, Ming Fu, Lingyun Wu, Rui Wang, Eden T Wondimu, Roberta Torregrossa, Zhuping Jin, Quanxi Zhang, Matthew Whiteman |
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| Rok vydání: | 2021 |
| Předmět: |
Erythrocytes
Physiology Clinical Biochemistry Endogeny Mitochondrion 7. Clean energy Mice 03 medical and health sciences Adenosine Triphosphate 0302 clinical medicine medicine Animals Glycolysis Hydrogen Sulfide Viability assay Hypoxia 030304 developmental biology Mammals 0303 health sciences Chemistry Cell Biology Metabolism Cell biology Red blood cell medicine.anatomical_structure 030220 oncology & carcinogenesis Erythropoiesis Intracellular |
| Zdroj: | Journal of Cellular Physiology. 237:763-773 |
| ISSN: | 1097-4652 0021-9541 |
| DOI: | 10.1002/jcp.30544 |
| Popis: | Hydrogen sulfide (H2 S) is a gasotransmitter that regulates both physiological and pathophysiological processes in mammalian cells. Recent studies have demonstrated that H2 S promotes aerobic energy production in the mitochondria in response to hypoxia, but its effect on anaerobic energy production has yet to be established. Glycolysis is the anaerobic process by which ATP is produced through the metabolism of glucose. Mammalian red blood cells (RBCs) extrude mitochondria and nucleus during erythropoiesis. These cells would serve as a unique model to observe the effect of H2 S on glycolysis-mediated energy production. The purpose of this study was to determine the effect of H2 S on glycolysis-mediated energy production in mitochondria-free mouse RBCs. Western blot analysis showed that the only H2 S-generating enzyme expressed in mouse RBCs is 3-mercaptopyruvate sulfurtransferase (MST). Supplement of the substrate for MST stimulated, but the inhibition of the same suppressed, the endogenous production of H2 S. Both exogenously administered H2 S salt and MST-derived endogenous H2 S stimulated glycolysis-mediated ATP production. The effect of NaHS on ATP levels was not affected by oxygenation status. On the contrary, hypoxia increased intracellular H2 S levels and MST activity in mouse RBCs. The mitochondria-targeted H2 S donor, AP39, did not affect ATP levels of mouse RBCs. NaHS at low concentrations (3-100 μM) increased ATP levels and decreased cell viability after 3 days of incubation in vitro. Higher NaHS concentrations (300-1000 μM) lowered ATP levels, but prolonged cell viability. H2 S may offer a cytoprotective effect in mammalian RBCs to maintain oxygen-independent energy production. |
| Databáze: | OpenAIRE |
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