Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/43604
Title: Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia.
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Issue Date: 2017
Citation: Redox Biol.2017 08;(12):1040-1051
Abstract: 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 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.
PMID: 28511347
URI: https://hdl.handle.net/20.500.12530/43604
Rights: openAccess
Appears in Collections:Hospitales > H. U. Santa Cristina > Artículos
Fundaciones e Institutos de Investigación > IIS H. U. La Princesa > Artículos

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