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|Title:||Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia.|
Electron Transport Complex I
|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.|
|Appears in Collections:||Hospitales > H. U. Santa Cristina > Artículos|
Fundaciones e Institutos de Investigación > IIS H. U. La Princesa > Artículos
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