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Difference between revisions of "Droese 2011 Mol Pharmacol"

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|injuries=Ischemia-Reperfusion; Preservation, RONS; Oxidative Stress
|injuries=Ischemia-Reperfusion; Preservation, RONS; Oxidative Stress
|organism=Rat
|organism=Rat
|tissues=Cardiac muscle
|tissues=Heart
|preparations=Isolated Mitochondria
|preparations=Isolated Mitochondria
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Revision as of 10:30, 27 February 2013

Publications in the MiPMap
Drรถse S, Bleier L, Brandt U (2011) A common mechanism links differently acting Complex II inhibitors to cardioprotection: modulation of mitochondrial reactive oxygen species production. Mol Pharmacol 79: 814-822.

ยป PMID:21278232

Droese S, Bleier L, Brandt U (2011) Mol Pharmacol

Abstract: In this study, we have analyzed the effect of different cardioprotective Complex II inhibitors on the mitochondrial production of reactive oxygen species (ROS) because ROS seem to be essential for signaling during preconditioning to prevent ischemia/reperfusion injury. Despite different binding sites and concentrations required for half-maximal inhibition-ranging from nanomolar for the Q site inhibitor atpenin A5 to millimolar for the succinate analog malonate-all inhibitors modulated ROS production in the same ambivalent fashion: they promoted the generation of superoxide at the Q(o) site of Complex III under conditions of "oxidant-induced reduction" but attenuated ROS generated at Complex I due to reverse electron transfer. All inhibitors showed these ambivalent effects independent of the presence of K(+). These findings suggest a direct modulation of mitochondrial ROS generation during cardioprotection via Complex II inhibition and question the recently proposed role of complex II as a regulatory component of the putative mitochondrial K(ATP) channel.


โ€ข O2k-Network Lab: DE Frankfurt Brandt U


Labels:

Stress:Ischemia-Reperfusion; Preservation"Ischemia-Reperfusion; Preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.  Organism: Rat  Tissue;cell: Heart  Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property. 



HRR: Oxygraph-2k