Different mechanisms of mitochondrial proton leak in ischaemia/reperfusion injury and preconditioning: implications for pathology and cardioprotection

The mechanisms of mitochondrial proton (H+) leak under various pathophysiological conditions are poorly understood. In the present study it was hypothesized that different mechanisms underlie H+ leak in cardiac IR (ischaemia/reperfusion) injury and IPC (ischaemic preconditioning). Potential H(+) lea...

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Bibliographic Details
Published in:Biochemical journal 2006-05, Vol.395 (3), p.611-618
Main Authors: Nadtochiy, Sergiy M, Tompkins, Andrew J, Brookes, Paul S
Format: Article
Language:English
Subjects:
Animals
Carrier Proteins - metabolism
Cell Membrane Permeability - drug effects
Guanosine Diphosphate - pharmacology
Ischemic Preconditioning, Myocardial
Male
Membrane Potentials - drug effects
Membrane Proteins - metabolism
Mitochondria, Heart - drug effects
Mitochondria, Heart - metabolism
Mitochondrial Membranes - drug effects
Mitochondrial Membranes - metabolism
Myocardial Reperfusion Injury - metabolism
Myocardial Reperfusion Injury - pathology
Myocardial Reperfusion Injury - physiopathology
Oxygen - metabolism
Protons
Rats
Rats, Sprague-Dawley
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Summary:The mechanisms of mitochondrial proton (H+) leak under various pathophysiological conditions are poorly understood. In the present study it was hypothesized that different mechanisms underlie H+ leak in cardiac IR (ischaemia/reperfusion) injury and IPC (ischaemic preconditioning). Potential H(+) leak mechanisms examined were UCPs (uncoupling proteins), allosteric activation of the ANT (adenine nucleotide translocase) by AMP, or the PT (permeability transition) pore. Mitochondria isolated from perfused rat hearts that were subjected to IPC exhibited a greater H+ leak than did controls (202+/-27%, P
ISSN:0264-6021
1470-8728
DOI:10.1042/BJ20051927