Nitrite Therapy After Cardiac Arrest Reduces Reactive Oxygen Species Generation, Improves Cardiac and Neurological Function, and Enhances Survival via Reversible Inhibition of Mitochondrial Complex I

2011 ◽  
Vol 2011 ◽  
pp. 220-222
Author(s):  
M. Mathru
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Arrest ◽  
Complex I ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Neurological Function ◽  
Mitochondrial Complex I ◽  
Oxygen Species ◽  
Mitochondrial Complex ◽  
Reversible Inhibition

scholarly journals Mammalian Mitochondrial Complex I: Biogenesis, Regulation, and Reactive Oxygen Species Generation

2010 ◽  
Vol 12 (12) ◽  
pp. 1431-1470 ◽  
Author(s):  
Werner J.H. Koopman ◽  
Leo G.J. Nijtmans ◽  
Cindy E.J. Dieteren ◽  
Peggy Roestenberg ◽  
Federica Valsecchi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Complex I ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Mitochondrial Complex I ◽  
Oxygen Species ◽  
Mitochondrial Complex

scholarly journals The Putative Drp1 Inhibitor mdivi-1 Is a Reversible Mitochondrial Complex I Inhibitor that Modulates Reactive Oxygen Species

2017 ◽  
Vol 40 (6) ◽  
pp. 583-594.e6 ◽  
Author(s):  
Evan A. Bordt ◽  
Pascaline Clerc ◽  
Brian A. Roelofs ◽  
Andrew J. Saladino ◽  
László Tretter ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Complex I ◽  
Reactive Oxygen ◽  
Mitochondrial Complex I ◽  
Oxygen Species ◽  
Mitochondrial Complex ◽  
Mitochondrial Complex I Inhibitor

Fluazinam targets mitochondrial complex I to induce reactive oxygen species-dependent cytotoxicity in SH-SY5Y cells

2012 ◽  
Vol 60 (8) ◽  
pp. 773-781 ◽  
Author(s):  
Jeong Eun Lee ◽  
Jin Sun Kang ◽  
Yeo-Woon Ki ◽  
Jae Hyeon Park ◽  
In Chul Shin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Complex I ◽  
Reactive Oxygen ◽  
Mitochondrial Complex I ◽  
Oxygen Species ◽  
Mitochondrial Complex

scholarly journals Physiologic Implications of Reactive Oxygen Species Production by Mitochondrial Complex I Reverse Electron Transport

Antioxidants ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 285 ◽  
Author(s):  
John O. Onukwufor ◽  
Brandon J. Berry ◽  
Andrew P. Wojtovich
Keyword(s):  
Reactive Oxygen Species ◽  
Electron Transport ◽  
Complex I ◽  
Reactive Oxygen ◽  
Reverse Direction ◽  
Mitochondrial Complex I ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Complex ◽  
Reverse Electron Transport

Mitochondrial reactive oxygen species (ROS) can be either detrimental or beneficial depending on the amount, duration, and location of their production. Mitochondrial complex I is a component of the electron transport chain and transfers electrons from NADH to ubiquinone. Complex I is also a source of ROS production. Under certain thermodynamic conditions, electron transfer can reverse direction and reduce oxygen at complex I to generate ROS. Conditions that favor this reverse electron transport (RET) include highly reduced ubiquinone pools, high mitochondrial membrane potential, and accumulated metabolic substrates. Historically, complex I RET was associated with pathological conditions, causing oxidative stress. However, recent evidence suggests that ROS generation by complex I RET contributes to signaling events in cells and organisms. Collectively, these studies demonstrate that the impact of complex I RET, either beneficial or detrimental, can be determined by the timing and quantity of ROS production. In this article we review the role of site-specific ROS production at complex I in the contexts of pathology and physiologic signaling.

Sign in / Sign up

Export Citation Format

Share Document