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L ‐Carnitine suppresses oleic acid‐induced membrane permeability transition of mitochondria
Author(s) -
Oyanagi Eri,
Yano Hiromi,
Kato Yasuko,
Fujita Hirofumi,
Utsumi Kozo,
Sasaki Junzo
Publication year - 2008
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1506
Subject(s) - carnitine , oleic acid , mitochondrion , chemistry , mitochondrial permeability transition pore , permeability (electromagnetism) , membrane , transition (genetics) , inner mitochondrial membrane , biophysics , membrane permeability , microbiology and biotechnology , biochemistry , biology , apoptosis , programmed cell death , gene
Membrane permeability transition (MPT) of mitochondria has an important role in apoptosis of various cells. The classic type of MPT is characterized by increased Ca 2+ transport, membrane depolarization, swelling, and sensitivity to cyclosporin A. In this study, we investigated whether L ‐carnitine suppresses oleic acid‐induced MPT using isolated mitochondria from rat liver. Oleic acid‐induced MPT in isolated mitochondria, inhibited endogenous respiration, caused membrane depolarization, and increased large amplitude swelling, and cytochrome c (Cyt. c ) release from mitochondria. L ‐Carnitine was indispensable to β ‐oxidation of oleic acid in the mitochondria, and this reaction required ATP and coenzyme A (CoA). In the presence of ATP and CoA, L ‐carnitine stimulated oleic acid oxidation and suppressed the oleic acid‐induced depolarization, swelling, and Cyt. c release. L ‐Carnitine also contributed to maintaining mitochondrial function, which was decreased by the generation of free fatty acids with the passage of time after isolation. These results suggest that L ‐carnitine acts to maintain mitochondrial function and suppresses oleic acid‐mediated MPT through acceleration of β ‐oxidation. Copyright © 2008 John Wiley & Sons, Ltd.