Hernansanz-Agustín, PabloRamos, ElenaNavarro, ElisaParada, EstherSánchez-López, NuriaPeláez-Aguado, LauraCabrera-García, J. DanielTello, DanielBuendia, IzaskunMarina, AnabelEgea, JavierLópez, Manuela G.Bogdanova, AnnaMartínez Ruiz, Antonio2024-04-112024-04-112017-082213-231710.1016/j.redox.2017.04.025https://hdl.handle.net/20.500.14352/103011Mitochondria 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.engAttribution-NonCommercial-NoDerivatives 4.0 Internationaljournal articleopen access577.1HypoxiaMitochondrial complex IRedox signallingOxygen sensingSuperoxideBioquímica (Farmacia)2302 Bioquímica