| Autor: |
Pablo Hernansanz-Agustín, Elena Ramos, Elisa Navarro, Esther Parada, Nuria Sánchez-López, Laura Peláez-Aguado, J. Daniel Cabrera-García, Daniel Tello, Izaskun Buendia, Anabel Marina, Javier Egea, Manuela G. López, Anna Bogdanova, Antonio Martínez-Ruiz |
| Jazyk: |
angličtina |
| Rok vydání: |
2017 |
| Předmět: |
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| Zdroj: |
Redox Biology, Vol 12, Iss , Pp 1040-1051 (2017) |
| Druh dokumentu: |
article |
| ISSN: |
2213-2317 |
| DOI: |
10.1016/j.redox.2017.04.025 |
| Popis: |
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. Keywords: Hypoxia, Oxygen sensing, Superoxide, Mitochondrial complex I, Redox signalling |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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