Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia

Redox Biology
Pablo Hernansanz-AgustínAntonio Martínez-Ruiz

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.

Citations

Feb 22, 2018·Cellular and Molecular Life Sciences : CMLS·Dominik C FuhrmannBernhard Brüne
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Jan 16, 2020·Biomolecules·Petr JežekLydie Plecitá-Hlavatá
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Mar 25, 2020·The Journal of Biological Chemistry·Jason J RoseMark T Gladwin
Jul 31, 2020·Nature·Pablo Hernansanz-AgustínAntonio Martínez-Ruiz
Nov 26, 2019·Biochemistry. Biokhimii︠a︡·A Galkin
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Methods Mentioned

BETA
transfection
fluorescence microscopy
electrophoresis
reverse phase chromatography
dissection
confocal microscopy

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