Impact of Hydrogen Sulfide on Mitochondrial and Bacterial Bioenergetics
This review focuses on the effects of hydrogen sulfide (H<sub>2</sub>S) on the unique bioenergetic molecular machines in mitochondria and bacteria—the protein complexes of electron transport chains and associated enzymes. H<sub>2</sub>S, along with nitric oxide and carbon mon...
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MDPI AG
2021-11-01
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author | Vitaliy B. Borisov Elena Forte |
author_facet | Vitaliy B. Borisov Elena Forte |
author_sort | Vitaliy B. Borisov |
collection | DOAJ |
description | This review focuses on the effects of hydrogen sulfide (H<sub>2</sub>S) on the unique bioenergetic molecular machines in mitochondria and bacteria—the protein complexes of electron transport chains and associated enzymes. H<sub>2</sub>S, along with nitric oxide and carbon monoxide, belongs to the class of endogenous gaseous signaling molecules. This compound plays critical roles in physiology and pathophysiology. Enzymes implicated in H<sub>2</sub>S metabolism and physiological actions are promising targets for novel pharmaceutical agents. The biological effects of H<sub>2</sub>S are biphasic, changing from cytoprotection to cytotoxicity through increasing the compound concentration. In mammals, H<sub>2</sub>S enhances the activity of F<sub>o</sub>F<sub>1</sub>-ATP (adenosine triphosphate) synthase and lactate dehydrogenase via their <i>S</i>-sulfhydration, thereby stimulating mitochondrial electron transport. H<sub>2</sub>S serves as an electron donor for the mitochondrial respiratory chain via sulfide quinone oxidoreductase and cytochrome <i>c</i> oxidase at low H<sub>2</sub>S levels. The latter enzyme is inhibited by high H<sub>2</sub>S concentrations, resulting in the reversible inhibition of electron transport and ATP production in mitochondria. In the branched respiratory chain of <i>Escherichia coli</i>, H<sub>2</sub>S inhibits the <i>bo</i><sub>3</sub> terminal oxidase but does not affect the alternative <i>bd</i>-type oxidases. Thus, in <i>E. coli</i> and presumably other bacteria, cytochrome <i>bd</i> permits respiration and cell growth in H<sub>2</sub>S-rich environments. A complete picture of the impact of H<sub>2</sub>S on bioenergetics is lacking, but this field is fast-moving, and active ongoing research on this topic will likely shed light on additional, yet unknown biological effects. |
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spelling | doaj.art-b5fa8fb6528248989f7450d86d8eba4d2023-11-23T02:26:26ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-11-0122231268810.3390/ijms222312688Impact of Hydrogen Sulfide on Mitochondrial and Bacterial BioenergeticsVitaliy B. Borisov0Elena Forte1Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Leninskie Gory, 119991 Moscow, RussiaDepartment of Biochemical Sciences, Sapienza University of Rome, 00185 Rome, ItalyThis review focuses on the effects of hydrogen sulfide (H<sub>2</sub>S) on the unique bioenergetic molecular machines in mitochondria and bacteria—the protein complexes of electron transport chains and associated enzymes. H<sub>2</sub>S, along with nitric oxide and carbon monoxide, belongs to the class of endogenous gaseous signaling molecules. This compound plays critical roles in physiology and pathophysiology. Enzymes implicated in H<sub>2</sub>S metabolism and physiological actions are promising targets for novel pharmaceutical agents. The biological effects of H<sub>2</sub>S are biphasic, changing from cytoprotection to cytotoxicity through increasing the compound concentration. In mammals, H<sub>2</sub>S enhances the activity of F<sub>o</sub>F<sub>1</sub>-ATP (adenosine triphosphate) synthase and lactate dehydrogenase via their <i>S</i>-sulfhydration, thereby stimulating mitochondrial electron transport. H<sub>2</sub>S serves as an electron donor for the mitochondrial respiratory chain via sulfide quinone oxidoreductase and cytochrome <i>c</i> oxidase at low H<sub>2</sub>S levels. The latter enzyme is inhibited by high H<sub>2</sub>S concentrations, resulting in the reversible inhibition of electron transport and ATP production in mitochondria. In the branched respiratory chain of <i>Escherichia coli</i>, H<sub>2</sub>S inhibits the <i>bo</i><sub>3</sub> terminal oxidase but does not affect the alternative <i>bd</i>-type oxidases. Thus, in <i>E. coli</i> and presumably other bacteria, cytochrome <i>bd</i> permits respiration and cell growth in H<sub>2</sub>S-rich environments. A complete picture of the impact of H<sub>2</sub>S on bioenergetics is lacking, but this field is fast-moving, and active ongoing research on this topic will likely shed light on additional, yet unknown biological effects.https://www.mdpi.com/1422-0067/22/23/12688hydrogen sulfidedonorsgasotransmittersmolecular bioenergeticsinhibitionelectron transport chain |
spellingShingle | Vitaliy B. Borisov Elena Forte Impact of Hydrogen Sulfide on Mitochondrial and Bacterial Bioenergetics International Journal of Molecular Sciences hydrogen sulfide donors gasotransmitters molecular bioenergetics inhibition electron transport chain |
title | Impact of Hydrogen Sulfide on Mitochondrial and Bacterial Bioenergetics |
title_full | Impact of Hydrogen Sulfide on Mitochondrial and Bacterial Bioenergetics |
title_fullStr | Impact of Hydrogen Sulfide on Mitochondrial and Bacterial Bioenergetics |
title_full_unstemmed | Impact of Hydrogen Sulfide on Mitochondrial and Bacterial Bioenergetics |
title_short | Impact of Hydrogen Sulfide on Mitochondrial and Bacterial Bioenergetics |
title_sort | impact of hydrogen sulfide on mitochondrial and bacterial bioenergetics |
topic | hydrogen sulfide donors gasotransmitters molecular bioenergetics inhibition electron transport chain |
url | https://www.mdpi.com/1422-0067/22/23/12688 |
work_keys_str_mv | AT vitaliybborisov impactofhydrogensulfideonmitochondrialandbacterialbioenergetics AT elenaforte impactofhydrogensulfideonmitochondrialandbacterialbioenergetics |