Xanthohumol induces generation of reactive oxygen species and triggers apoptosis through inhibition of mitochondrial electron transfer chain complex I

2015 ◽  
Vol 89 ◽  
pp. 486-497 ◽  
Author(s):  
Bo Zhang ◽  
Wei Chu ◽  
Peng Wei ◽  
Ying Liu ◽  
Taotao Wei
Keyword(s):  
Reactive Oxygen Species ◽  
Electron Transfer ◽  
Complex I ◽  
Reactive Oxygen ◽  
Chain Complex ◽  
Oxygen Species ◽  
Electron Transfer Chain ◽  
Transfer Chain

Cadmium inhibits the electron transfer chain and induces Reactive Oxygen Species

2004 ◽  
Vol 36 (11) ◽  
pp. 1434-1443 ◽  
Author(s):  
Yudong Wang ◽  
Jing Fang ◽  
Stephen S Leonard ◽  
K.Murali Krishna Rao
Keyword(s):  
Reactive Oxygen Species ◽  
Electron Transfer ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Electron Transfer Chain ◽  
Transfer Chain

scholarly journals Oxygen Sensitivity of Mitochondrial Reactive Oxygen Species Generation Depends on Metabolic Conditions

2009 ◽  
Vol 284 (24) ◽  
pp. 16236-16245 ◽  
Author(s):  
David L. Hoffman ◽  
Paul S. Brookes
Keyword(s):  
Reactive Oxygen Species ◽  
Electron Transfer ◽  
Complex I ◽  
Reactive Oxygen ◽  
Complex Iii ◽  
Ros Generation ◽  
Oxygen Species ◽  
Quinone Oxidoreductase ◽  
Electron Transfer Flavoprotein ◽  
Metabolic Conditions

The mitochondrial generation of reactive oxygen species (ROS) plays a central role in many cell signaling pathways, but debate still surrounds its regulation by factors, such as substrate availability, [O2] and metabolic state. Previously, we showed that in isolated mitochondria respiring on succinate, ROS generation was a hyperbolic function of [O2]. In the current study, we used a wide variety of substrates and inhibitors to probe the O2 sensitivity of mitochondrial ROS generation under different metabolic conditions. From such data, the apparent Km for O2 of putative ROS-generating sites within mitochondria was estimated as follows: 0.2, 0.9, 2.0, and 5.0 μm O2 for the complex I flavin site, complex I electron backflow, complex III QO site, and electron transfer flavoprotein quinone oxidoreductase of β-oxidation, respectively. Differential effects of respiratory inhibitors on ROS generation were also observed at varying [O2]. Based on these data, we hypothesize that at physiological [O2], complex I is a significant source of ROS, whereas the electron transfer flavoprotein quinone oxidoreductase may only contribute to ROS generation at very high [O2]. Furthermore, we suggest that previous discrepancies in the assignment of effects of inhibitors on ROS may be due to differences in experimental [O2]. Finally, the data set (see supplemental material) may be useful in the mathematical modeling of mitochondrial metabolism.

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