| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10800938 | Biochimica et Biophysica Acta (BBA) - General Subjects | 2009 | 8 Pages |
Abstract
A straightforward rationale is presented to mechanistically explain the ambivalent effects of diazoxide reported in the literature. Depending on the metabolic state and the membrane potential of mitochondria, diazoxide-mediated inhibition of complex II promotes transient generation of signaling ROS at complex III (during preconditioning) or attenuates the production of deleterious ROS at complex I (during ischemia and reperfusion).
Keywords
5-HDQ-pool2-n-decyl-quinazolin-4-yl-aminen-decylubiquinoneDQADBQpharmacological preconditioningRHM5-hydroxydecanoateFCCPRCFHRPDBHSMPSROSdiazoxideSubmitochondrial particlesRespiratory chainSODSuperoxide dismutaseRedox signalingRat heart mitochondriaMitochondriaHorseradish peroxidaseTCA cycleReactive oxygen species
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Authors
Stefan Dröse, Peter J. Hanley, Ulrich Brandt,