Journal
REDOX BIOLOGY
Volume 12, Issue -, Pages 1040-1051Publisher
ELSEVIER
DOI: 10.1016/j.redox.2017.04.025
Keywords
Hypoxia; Oxygen sensing; Superoxide; Mitochondrial complex I; Redox signalling
Categories
Funding
- Spanish Government - European Union FEDER/ERDF (RosasNet, Consolider-Ingenio programme) [CSD2007-00020]
- Consolredox network [SAF2015-71521-REDC, PI12/00875, PI15/00107]
- Fundacion Domingo Martinez (Ayuda a la Investigacion Area de Biomedicina y Salud) [SAF2013-32223]
- Swiss National Science Foundation (SNF) [310030_124970/1]
- Instituto de Investigacion Sanitaria Princesa (Ayuda para estancia breve)
- COST actions [TD0901, BM1203]
- Spanish Government [AP2010-1219, AP2012-5621]
- Universidad Autonoma de Madrid (UAM) [FPI-UAM2012]
- I3SNS
- Miguel Servet programmes (ISCIII, Spanish Government) [CES12/005, CP14/00008]
- FEDER/ERDF
- Swiss National Science Foundation (SNF) [310030_124970] Funding Source: Swiss National Science Foundation (SNF)
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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.
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