ArticleThe Journal of biological chemistry2012
The deactive form of respiratory complex I from mammalian mitochondria is a Na+/H+ antiporter.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 85 citations in OpenAlex.
- A ratiometric fluorescent reporter of mitochondrial sodium.Nature chemical biology · 2026Article
- Targeting the Electron Transport System for Enhanced Longevity.Biomolecules · 2025Review
- Novel findings on the mitochondria in ciliates, with description of mitochondrial genomes of six representatives.Marine life science & technology · 2025Article
- Potential for flexible lactate shuttling between astrocytes and neurons to mitigate against diving-induced hypoxia.Frontiers in neuroanatomy · 2025Article
- Using light scattering to assess how phospholipid-protein interactions affect complex I functionality in liposomes.RSC chemical biology · 2023Article
- Transgenic NADH dehydrogenase restores oxygen regulation of breathing in mitochondrial complex I-deficient mice.Nature communications · 2023Article
- Binding of Natural Inhibitors to Respiratory Complex I.Pharmaceuticals (Basel, Switzerland) · 2022Review
- ND3 Cys39 in complex I is exposed during mitochondrial respiration.Cell chemical biology · 2022Article
- Reverse Electron Transfer by Respiratory Complex I Catalyzed in a Modular Proteoliposome System.Journal of the American Chemical Society · 2022Article
- Bioactivity of Inhaled Methane and Interactions With Other Biological Gases.Frontiers in cell and developmental biology · 2021Review
- Ubiquinone Binding and Reduction by Complex I-Open Questions and Mechanistic Implications.Frontiers in chemistry · 2021Review
- Functional Water Wires Catalyze Long-Range Proton Pumping in the Mammalian Respiratory Complex I.Journal of the American Chemical Society · 2020Article
- SQR mediates therapeutic effects of HScience advances · 2020Article
- Bottom-Up Construction of a Minimal System for Cellular Respiration and Energy Regeneration.ACS synthetic biology · 2020Article
- Mitochondrial respiratory chain composition and organization in response to changing oxygen levels.Journal of life sciences (Westlake Village, Calif.) · 2020Article
- Brain Ischemia/Reperfusion Injury and Mitochondrial Complex I Damage.Biochemistry. Biokhimiia · 2019Review
- Mitochondrial Oxidative Phosphorylation defect in the Heart of Subjects with Coronary Artery Disease.Scientific reports · 2019Article
- Mitochondrial Dysfunctions: A Thread Sewing Together Alzheimer's Disease, Diabetes, and Obesity.Oxidative medicine and cellular longevity · 2019Review
- Locking loop movement in the ubiquinone pocket of complex I disengages the proton pumps.Nature communications · 2018Article
- Long-range proton-coupled electron transfer in biological energy conversion: towards mechanistic understanding of respiratory complex I.Journal of the Royal Society, Interface · 2018Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In mitochondria, complex I (NADH:ubiquinone oxidoreductase) uses the redox potential energy from NADH oxidation by ubiquinone to transport protons across the inner membrane, contributing to the proton-motive force. However, in some prokaryotes, complex I may transport sodium ions instead, and three subunits in the membrane domain of complex I are closely related to subunits from the Mrp family of Na(+)/H(+) antiporters. Here, we define the relationship between complex I from Bos taurus heart mitochondria, a close model for the human enzyme, and sodium ion transport across the mitochondrial inner membrane. In accord with current consensus, we exclude the possibility of redox-coupled Na(+) transport by B. taurus complex I. Instead, we show that the "deactive" form of complex I, which is formed spontaneously when enzyme turnover is precluded by lack of substrates, is a Na(+)/H(+) antiporter. The antiporter activity is abolished upon reactivation by the addition of substrates and by the complex I inhibitor rotenone. It is specific for Na(+) over K(+), and it is not exhibited by complex I from the yeast Yarrowia lipolytica, which thus has a less extensive deactive transition. We propose that the functional connection between the redox and transporter modules of complex I is broken in the deactive state, allowing the transport module to assert its independent properties. The deactive state of complex I is formed during hypoxia, when respiratory chain turnover is slowed, and may contribute to determining the outcome of ischemia-reperfusion injury.
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Registered trials
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