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Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia

AuthorsHernansanz-Agustín, Pablo; Ramos, Elena; Navarro, Elisa; Parada, Esther; Sánchez-López, Nuria; Peláez-Aguado, Laura; Cabrera-García, Daniel J.; Tello, Daniel; Buendía Abaitua, Izaskun; Marina, Anabel ; Egea Maiquez, Javier; López, Manuela G.; Bogdanova, Anna; Martínez-Ruiz, Antonio
KeywordsRedox signalling
Mitochondrial complex I
Oxygen sensing
Issue Date21-Apr-2017
CitationRedox Biology 12: 1040- 1051 (2017)
AbstractMitochondria use oxygen as the final acceptor of the respiratory chain, but its incomplete reduction can also produce reactive oxygen species (ROS), especially superoxide. Acute hypoxia produces a superoxide burst in different cell types, but the triggering mechanism is still unknown. Herein, we show that complex I is involved in this superoxide burst under acute hypoxia in endothelial cells. We have also studied the possible mechanisms by which complex I could be involved in this burst, discarding reverse electron transport in complex I and the implication of PTEN-induced putative kinase 1 (PINK1). We show that complex I transition from the active to ‘deactive’ form is enhanced by acute hypoxia in endothelial cells and brain tissue, and we suggest that it can trigger ROS production through its Na/H antiporter activity. These results highlight the role of complex I as a key actor in redox signalling in acute hypoxia.
Publisher version (URL)https://doi.org/10.1016/j.redox.2017.04.025
Identifiersdoi: 10.1016/j.redox.2017.04.025
issn: 2213-2317
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