Cited by 222Nitric Oxide and Endothelin EffectsMitochondrial Function and PathologyCardiac Ischemia and Reperfusion

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A mitochondria-targeted S -nitrosothiol modulates respiration, nitrosates thiols, and protects against ischemia-reperfusion injury

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Prime, Tracy A., Blaikie, Frances H., Evans, Cameron, Nadtochiy, Sergiy M., James, Andrew M., Dahm, Christina C., Vitturi, Dario A., Patel, Rakesh P., Hiley, C. Robin, Abakumova, Irina, Requejo, Raquel, Chouchani, Edward T., Hurd, Thomas R., Garvey, John F., Taylor, Cormac T., Brookes, Paul S., Smith, Robin A. J., Murphy, Michael P.·2009·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.0903250106PMC PMC2696550

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Abstract

Nitric oxide (NO • ) competitively inhibits oxygen consumption by mitochondria at cytochrome c oxidase and S -nitrosates thiol proteins. We developed mitochondria-targeted S -nitrosothiols (MitoSNOs) that selectively modulate and protect mitochondrial function. The exemplar MitoSNO1, produced by covalently linking an S -nitrosothiol to the lipophilic triphenylphosphonium cation, was rapidly and extensively accumulated within mitochondria, driven by the membrane potential, where it generated NO • and S -nitrosated thiol proteins. MitoSNO1-induced NO • production reversibly inhibited respiration at cytochrome c oxidase and increased extracellular oxygen concentration under hypoxic conditions. MitoSNO1 also caused vasorelaxation due to its NO • generation. Infusion of MitoSNO1 during reperfusion was protective against heart ischemia-reperfusion injury, consistent with a functional modification of mitochondrial proteins, such as complex I, following S -nitrosation. These results support the idea that selectively targeting NO • donors to mitochondria is an effective strategy to reversibly modulate respiration and to protect mitochondria against ischemia-reperfusion injury.

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Authors: Prime, T. A., Blaikie, F. H., Evans, C., Nadtochiy, S. M., James, A. M., Dahm, C. C., Vitturi, D. A., Patel, R. P., Hiley, C. R., Abakumova, I., Requejo, R., Chouchani, E. T., Hurd, T. R., Garvey, J. F., Taylor, C. T., Brookes, P. S., Smith, R. A. J., & Murphy, M. P.
Affiliations: MRC Mitochondrial Biology Unit (GB)
University of Otago (NZ)
University of Rochester Medicine (US)
Department of Pathology and Center for Free Radical Biology, University of Alabama at Birmingham, 901 19th Street South, Birmingham, AL 35294;
University of Alabama at Birmingham (US)
University of Cambridge (GB)
MRC Mitochondrial Biology Unit, Hills Road, Cambridge CB2 0XY, United Kingdom;
University College Dublin (IE)
ORCID: Blaikie, Frances H.
Nadtochiy, Sergiy M.
James, Andrew M.
Dahm, Christina C.
Patel, Rakesh P.
Hiley, C. Robin
Chouchani, Edward T.
Hurd, Thomas R.
Garvey, John F.
Taylor, Cormac T.
Brookes, Paul S.
Murphy, Michael P.
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2009-06-30
Volume: 106
Issue: 26
Pages: 10764-10769
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.0903250106
PMC: PMC2696550
OpenAlex: W2061490621
Cited by: 222
References: 20
Citations by year: 2026: 2 · 2025: 8 · 2024: 7 · 2023: 9 · 2022: 11 · 2021: 8 · 2020: 11 · 2019: 8 · 2018: 11 · 2017: 9 · 2016: 16 · 2015: 11 · 2014: 28 · 2013: 24 · 2012: 18
FWCI: 13.03
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: University of Otago
Health Research Board
Science Foundation Ireland
National Institutes of Health
Medical Research Council
National Heart, Lung, and Blood Institute (HL-071158, R01HL071158)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Keywords: nitric oxide, S-nitrosylation, cytochrome c oxidase inhibition, mitochondrial respiration, ischemia-reperfusion injury, heart protection, triphenylphosphonium, membrane potential, hypoxia, vasorelaxation, complex I, mitochondrial proteins
MeSH terms: Animals, Aorta, Thoracic, Cell Line, Heart, HeLa Cells, Humans, Male, Mice, Inbred C57BL, Mitochondria, Mitochondria, Heart, Nitric Oxide, Oxygen Consumption, Mass Spectrometry, Sulfhydryl Compounds, Vasodilation, Reperfusion Injury, Nitrosation, Rats, Sprague-Dawley, S-Nitrosothiols, Myoblasts, Electron Transport Complex I, Mice, Rats, Membrane Potential, Mitochondrial, In Vitro Techniques

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A mitochondria-targeted S -nitrosothiol modulates respiration, nitrosates thiols, and protects against ischemia-reperfusion injury

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