Mitochondrial complex I.

TitleMitochondrial complex I.
Publication TypeJournal Article
Year of Publication2013
AuthorsHirst, J
JournalAnnu Rev Biochem
Volume82
Pagination551-75
Date Published2013
ISSN1545-4509
KeywordsElectron Transport, Electron Transport Complex I, Flavins, Humans, Mitochondria, Oxidation-Reduction, Reactive Oxygen Species, Ubiquinone
Abstract

Complex I (NADH:ubiquinone oxidoreductase) is crucial for respiration in many aerobic organisms. In mitochondria, it oxidizes NADH from the tricarboxylic acid cycle and β-oxidation, reduces ubiquinone, and transports protons across the inner membrane, contributing to the proton-motive force. It is also a major contributor to cellular production of reactive oxygen species. The redox reaction of complex I is catalyzed in the hydrophilic domain; it comprises NADH oxidation by a flavin mononucleotide, intramolecular electron transfer along a chain of iron-sulfur clusters, and ubiquinone reduction. Redox-coupled proton translocation in the membrane domain requires long-range energy transfer through the protein complex, and the molecular mechanisms that couple the redox and proton-transfer half-reactions are currently unknown. This review evaluates extant data on the mechanisms of energy transduction and superoxide production by complex I, discusses contemporary mechanistic models, and explores how mechanistic studies may contribute to understanding the roles of complex I dysfunctions in human diseases.

DOI10.1146/annurev-biochem-070511-103700
Alternate JournalAnnu. Rev. Biochem.
Citation Key10.1146/annurev-biochem-070511-103700
PubMed ID23527692
Grant ListMC_U105663141 / / Medical Research Council / United Kingdom