Mechanism of mitochondrial complex I damage in brain ischemia/reperfusion injury. A hypothesis

2019 ◽  
Vol 100 ◽  
pp. 103408 ◽  
Author(s):  
Vadim Ten ◽  
Alexander Galkin
Keyword(s):  
Reperfusion Injury ◽  
Brain Ischemia ◽  
Complex I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex

scholarly journals Redox-Dependent Loss of Flavin by Mitochondrial Complex I in Brain Ischemia/Reperfusion Injury

2019 ◽  
Vol 31 (9) ◽  
pp. 608-622 ◽  
Author(s):  
Anna Stepanova ◽  
Sergey Sosunov ◽  
Zoya Niatsetskaya ◽  
Csaba Konrad ◽  
Anatoly A. Starkov ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Brain Ischemia ◽  
Complex I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex

scholarly journals Reverse electron transfer results in a loss of flavin from mitochondrial complex I: Potential mechanism for brain ischemia reperfusion injury

2017 ◽  
Vol 37 (12) ◽  
pp. 3649-3658 ◽  
Author(s):  
Anna Stepanova ◽  
Anja Kahl ◽  
Csaba Konrad ◽  
Vadim Ten ◽  
Anatoly S Starkov ◽  
...  
Keyword(s):  
Electron Transfer ◽  
Brain Ischemia ◽  
Complex I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Brain Mitochondria ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Reverse Electron Transfer ◽  
Novel Target

Ischemic stroke is one of the most prevalent sources of disability in the world. The major brain tissue damage takes place upon the reperfusion of ischemic tissue. Energy failure due to alterations in mitochondrial metabolism and elevated production of reactive oxygen species (ROS) is one of the main causes of brain ischemia-reperfusion (IR) damage. Ischemia resulted in the accumulation of succinate in tissues, which favors the process of reverse electron transfer (RET) when a fraction of electrons derived from succinate is directed to mitochondrial complex I for the reduction of matrix NAD+. We demonstrate that in intact brain mitochondria oxidizing succinate, complex I became damaged and was not able to contribute to the physiological respiration. This process is associated with a decline in ROS release and a dissociation of the enzyme's flavin. This previously undescribed phenomenon represents the major molecular mechanism of injury in stroke and induction of oxidative stress after reperfusion. We also demonstrate that the origin of ROS during RET is flavin of mitochondrial complex I. Our study highlights a novel target for neuroprotection against IR brain injury and provides a sensitive biochemical marker for this process.

scholarly journals Steatotic livers are susceptible to normothermic ischemia-reperfusion injury from mitochondrial Complex-I dysfunction

2016 ◽  
Vol 22 (19) ◽  
pp. 4673 ◽  
Author(s):  
Michael JJ Chu ◽  
Rakesh Premkumar ◽  
Anthony JR Hickey ◽  
Yannan Jiang ◽  
Brett Delahunt ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Complex I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex

scholarly journals Suppressors of Superoxide-H 2 O 2 Production at Site I Q of Mitochondrial Complex I Protect against Stem Cell Hyperplasia and Ischemia-Reperfusion Injury

2016 ◽  
Vol 24 (4) ◽  
pp. 582-592 ◽  
Author(s):  
Martin D. Brand ◽  
Renata L.S. Goncalves ◽  
Adam L. Orr ◽  
Leonardo Vargas ◽  
Akos A. Gerencser ◽  
...  
Keyword(s):  
Stem Cell ◽  
Reperfusion Injury ◽  
Complex I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Cell Hyperplasia

scholarly journals Decreased nitration of mitochondrial complex I by ROS/RNS scavenging during cardiac ischemia reperfusion injury

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Qunli Cheng ◽  
Meiying Yang ◽  
James S Heisner ◽  
Martin Bienengraeber ◽  
Wai‐Meng Kwok ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Complex I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex
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