ArticleBiochemical Society transactions2013
Molecular mechanism and physiological role of active-deactive transition of mitochondrial complex I.
Article in Biochemical Society transactions, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 34 citations in OpenAlex.
- Nrf1 acts as a highly-conserved determinon for maintaining robust redox homeostasis in the eco-evo-devo process of life histories.Cell stress · 2025Review
- Complex I activity in hypoxia: implications for oncometabolism.Biochemical Society transactions · 2024Review
- Residual Complex I activity and amphidirectional Complex II operation support glutamate catabolism through mtSLP in anoxia.Scientific reports · 2024Article
- A New Quinone-Based Inhibitor of Mitochondrial Complex I in D-Conformation, Producing Invasion Reduction and Sensitization to Venetoclax in Breast Cancer Cells.Antioxidants (Basel, Switzerland) · 2023Article
- Transgenic NADH dehydrogenase restores oxygen regulation of breathing in mitochondrial complex I-deficient mice.Nature communications · 2023Article
- Deactivation blocks proton pathways in the mitochondrial complex I.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Leigh Syndrome: A Tale of Two Genomes.Frontiers in physiology · 2021Review
- Brain Ischemia/Reperfusion Injury and Mitochondrial Complex I Damage.Biochemistry. Biokhimiia · 2019Review
- Deactivation of mitochondrial complex I after hypoxia-ischemia in the immature brain.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Mitochondrial Oxidative Phosphorylation defect in the Heart of Subjects with Coronary Artery Disease.Scientific reports · 2019Article
- Mitochondrial Complex I Inhibition by Metformin Limits Reperfusion Injury.The Journal of pharmacology and experimental therapeutics · 2019Article
- Article
- Molecular dynamics and structural models of the cyanobacterial NDH-1 complex.Biochimica et biophysica acta. Bioenergetics · 2019Article
- The Roles of p53 in Mitochondrial Dynamics and Cancer Metabolism: The Pendulum between Survival and Death in Breast Cancer?Cancers · 2018Review
- Long-range proton-coupled electron transfer in biological energy conversion: towards mechanistic understanding of respiratory complex I.Journal of the Royal Society, Interface · 2018Review
- Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia.Redox biology · 2017Article
- Modulation of the conformational state of mitochondrial complex I as a target for therapeutic intervention.Interface focus · 2017Review
- Ischemic A/D transition of mitochondrial complex I and its role in ROS generation.Biochimica et biophysica acta · 2016Review
- Effect of monovalent cations on the kinetics of hypoxic conformational change of mitochondrial complex I.Biochimica et biophysica acta · 2015Article
- Pivotal Importance of STAT3 in Protecting the Heart from Acute and Chronic Stress: New Advancement and Unresolved Issues.Frontiers in cardiovascular medicine · 2015Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
The unique feature of mitochondrial complex I is the so-called A/D transition (active-deactive transition). The A-form catalyses rapid oxidation of NADH by ubiquinone (k ~104 min-1) and spontaneously converts into the D-form if the enzyme is idle at physiological temperatures. Such deactivation occurs in vitro in the absence of substrates or in vivo during ischaemia, when the ubiquinone pool is reduced. The D-form can undergo reactivation given both NADH and ubiquinone availability during slow (k ~1-10 min-1) catalytic turnover(s). We examined known conformational differences between the two forms and suggested a mechanism exerting A/D transition of the enzyme. In addition, we discuss the physiological role of maintaining the enzyme in the D-form during the ischaemic period. Accumulation of the D-form of the enzyme would prevent reverse electron transfer from ubiquinol to FMN which could lead to superoxide anion generation. Deactivation would also decrease the initial burst of respiration after oxygen reintroduction. Therefore the A/D transition could be an intrinsic protective mechanism for lessening oxidative damage during the early phase of reoxygenation. Exposure of Cys39 of mitochondrially encoded subunit ND3 makes the D-form susceptible for modification by reactive oxygen species and nitric oxide metabolites which arrests the reactivation of the D-form and inhibits the enzyme. The nature of thiol modification defines deactivation reversibility, the reactivation timescale, the status of mitochondrial bioenergetics and therefore the degree of recovery of the ischaemic tissues after reoxygenation.
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