Faculty Opinions recommendation of Qo site of mitochondrial complex III is the source of increased superoxide after transient exposure to hydrogen peroxide.

Author(s):  
Dirk van Helden ◽  
Mohammad Imtiaz
2014 ◽  
Vol 1840 (7) ◽  
pp. 2212-2221 ◽  
Author(s):  
An-Hui Gao ◽  
Yan-Yun Fu ◽  
Kun-Zhi Zhang ◽  
Mei Zhang ◽  
Hao-Wen Jiang ◽  
...  

2020 ◽  
Vol 236 (4) ◽  
pp. 2920-2933
Author(s):  
Meng Gao ◽  
Yuan Qin ◽  
Anqi Li ◽  
Sailei Wei ◽  
Bilin Liu ◽  
...  

2019 ◽  
Vol 47 (5) ◽  
pp. 1461-1469 ◽  
Author(s):  
Mark A. Watson ◽  
Hoi-Shan Wong ◽  
Martin D. Brand

Abstract Changes in mitochondrial superoxide and hydrogen peroxide production may contribute to various pathologies, and even aging, given that over time and in certain conditions, they damage macromolecules and disrupt normal redox signalling. Mitochondria-targeted antioxidants such as mitoQ, mitoVitE, and mitoTEMPO have opened up the study of the importance of altered mitochondrial matrix superoxide/hydrogen peroxide in disease. However, the use of such tools has caveats and they are unable to distinguish precise sites of production within the reactions of substrate oxidation and the electron transport chain. S1QELs are specific small-molecule Suppressors of site IQElectron Leak and S3QELs are specific small-molecule Suppressors of site IIIQoElectron Leak; they prevent superoxide/hydrogen production at specific sites without affecting electron transport or oxidative phosphorylation. We discuss the benefits of using S1QELs and S3QELs as opposed to mitochondria-targeted antioxidants, mitochondrial poisons, and genetic manipulation. We summarise pathologies in which site IQ in mitochondrial complex I and site IIIQo in mitochondrial complex III have been implicated using S1QELs and S3QELs.


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