Document Detail

Prevention of I/R injury in fatty livers by ischemic preconditioning is associated with increased mitochondrial tolerance: the key role of ATPsynthase and mitochondrial permeability transition.
MedLine Citation:
PMID:  19619169     Owner:  NLM     Status:  MEDLINE    
Ischemia/reperfusion (I/R) injury is a commonly encountered clinical problem and occurs probably as a consequence of irreversible mitochondrial injury. The increased susceptibility of fatty livers to ischemic injury is associated with depletion of adenosine triphosphate (ATP) content, which is preserved by preconditioning. Mitochondria being the main ATP production source for the cell, we aimed to evaluate whether ischemic preconditioning (IPC) of fatty livers prevents the impairment in mitochondrial function induced by I/R. Lean and steatotic animals were subjected to 90 min of hepatic warm ischemia and 12 h of reperfusion. IPC effect was tested in fatty livers. After reperfusion, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured. Mitochondrial membrane potential, mitochondrial respiration and susceptibility to mitochondrial permeability transition (MPT) were evaluated, as well as ATPase activity and adenine nucleotides. IPC of fatty livers decreased serum AST and ALT levels. Fatty animals subjected to I/R exhibited decreased mitochondrial membrane potential and a delay in the repolarization after a phosphorylation cycle, associated with increased state 4 respiration. Increased tolerance to MPT induction, preservation of F(1)F(o)-ATPsynthase activity and mitochondrial bioenergetics were observed in ischemic preconditioned fatty livers. Thus, IPC is an endogenous protecting mechanism that preserves mitochondrial function and bioenergetics in fatty livers.
Anabela Pinto Rolo; João Soeiro Teodoro; Carmen Peralta; Joan Rosello-Catafau; Carlos M Palmeira
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-07-10
Journal Detail:
Title:  Transplant international : official journal of the European Society for Organ Transplantation     Volume:  22     ISSN:  1432-2277     ISO Abbreviation:  Transpl. Int.     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2009-10-05     Completed Date:  2009-12-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8908516     Medline TA:  Transpl Int     Country:  England    
Other Details:
Languages:  eng     Pagination:  1081-90     Citation Subset:  IM    
Center for Neurosciences and Cell Biology, Department of Zoology, University of Coimbra, Coimbra, Portugal.
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MeSH Terms
Adenosine Triphosphate / metabolism
Alanine Transaminase / blood
Aspartate Aminotransferases / blood
Choline Deficiency / complications
Fatty Liver / complications*,  enzymology,  etiology,  physiopathology
Ischemic Preconditioning*
Membrane Potential, Mitochondrial
Mitochondria, Liver / enzymology,  physiology*
Mitochondrial Membrane Transport Proteins / physiology
Mitochondrial Proton-Translocating ATPases / physiology*
Oxygen Consumption
Random Allocation
Rats, Wistar
Reperfusion Injury / prevention & control*
Reg. No./Substance:
0/Mitochondrial Membrane Transport Proteins; 0/mitochondrial permeability transition pore; 56-65-5/Adenosine Triphosphate; EC Aminotransferases; EC Transaminase; EC 3.6.3.-/Mitochondrial Proton-Translocating ATPases

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