%0 Journal Article
%A Hernansanz-Agustín, Pablo
%A Ramos, Elena
%A Navarro, Elisa
%A Parada, Esther
%A Sánchez-López, Nuria
%A Peláez-Aguado, Laura
%A Cabrera-García, J. Daniel
%A Tello, Daniel
%A Buendia, Izaskun
%A Marina, Anabel
%A Egea, Javier
%A López, Manuela G.
%A Bogdanova, Anna
%A Martínez Ruiz, Antonio
%T Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia
%D 2017
%@ 2213-2317
%U https://hdl.handle.net/20.500.14352/103011
%X Mitochondria 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 bywhich 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.
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