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10.1016/j.redox.2017.04.025 http://scihub22266oqcxt.onion/10.1016/j.redox.2017.04.025 C5430576!5430576!28511347     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Redox+Biol 2017 ; 12 (ä): 1040-51 Nephropedia Template TP {{tp|p=28511347|t=2017. Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia |pdf=|usr=}}{{28511347}} gab.com Text Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia JO: Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=28511347 #FOAvip 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. Twit Text FOAVip Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia ????Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=28511347 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28511347 #FOAvip English Wikipedia <ref>{{Cite pmid|28511347}}</ref> Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia #MMPMID28511347 Hernansanz-Agustín P; Ramos E; Navarro E; Parada E; Sánchez-López N; Peláez-Aguado L; Cabrera-García JD; Tello D; Buendia I; Marina A; Egea J; López MG; Bogdanova A; Martínez-Ruiz A Redox Biol 2017[Aug]; 12 (ä): 1040-51 PMID28511347show ga 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. äMitochondrial complex I deactivation is related to superoxide producti(epmc).pdf DeepDyve Pubget Overpricing