Difference between revisions of "Hoffman 2009 J Biol Chem"
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{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration | ||
|injuries=Oxidative stress;RONS | |||
|organism=Rat | |organism=Rat | ||
|preparations=Isolated mitochondria | |preparations=Isolated mitochondria | ||
|enzymes=Complex I, Complex III, TCA cycle and matrix dehydrogenases | |enzymes=Complex I, Complex III, TCA cycle and matrix dehydrogenases | ||
|topics=Oxygen kinetics, Redox state | |topics=Oxygen kinetics, Redox state | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|additional=MitoFit 2021 AmR | |||
}} | }} |
Revision as of 15:40, 31 May 2021
Hoffman DL, Brookes PS (2009) Oxygen sensitivity of mitochondrial reactive oxygen species generation depends on metabolic conditions. J Biol Chem 284:16236-45. |
Hoffman DL, Brookes PS (2009) J Biol Chem
Abstract: 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 microM O2 for the complex I flavin site, complex I electron backflow, complex III QO site, and electron transfer flavoprotein quinone oxidoreductase of beta-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.
Labels: MiParea: Respiration
Stress:Oxidative stress;RONS Organism: Rat
Preparation: Isolated mitochondria Enzyme: Complex I, Complex III, TCA cycle and matrix dehydrogenases Regulation: Oxygen kinetics, Redox state Coupling state: OXPHOS
MitoFit 2021 AmR