RT Journal Article
T1 Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia
A1 Hernansanz-Agustín, Pablo
A1 Ramos, Elena
A1 Navarro, Elisa
A1 Parada, Esther
A1 Sánchez-López, Nuria
A1 Peláez-Aguado, Laura
A1 Cabrera-García, J. Daniel
A1 Tello, Daniel
A1 Buendia, Izaskun
A1 Marina, Anabel
A1 Egea, Javier
A1 López, Manuela G.
A1 Bogdanova, Anna
A1 Martínez Ruiz, Antonio
AB 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.
SN 2213-2317
YR 2017
FD 2017-08
LK https://hdl.handle.net/20.500.14352/103011
UL https://hdl.handle.net/20.500.14352/103011
LA eng
NO Spanish Government
NO Fundación Domingo Martínez
NO European Union FEDER/ERDF
NO Swiss National Science Foundation
NO Instituto de Investigación Sanitaria Princesa
NO Universidad Autónoma de Madrid
DS Docta Complutense
RD 7 oct 2024