L-Carnitine suppresses oleic acid-induced membrane permeability transition of mitochondria

Authors

  • Eri Oyanagi,

    1. Department of Cytology & Histology, Okayama University Graduate School, Medicine, Dentistry and Pharmaceutical Sciences, Shikata, Okayama, Japan
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  • Hiromi Yano,

    Corresponding author
    1. Department of Health & Sports Science, Kawasaki University of Medical Welfare, Matsushima, Kurashiki, Japan
    • Department of Health and Sports Science, Kawasaki University of Medical Welfare, 288 Matsushima, Kurashiki, Okayama 701-0193, Japan.
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  • Yasuko Kato,

    1. Department of Clinical Nutrition, Kawasaki University of Medical Welfare, Matsushima, Kurashiki, Japan
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  • Hirofumi Fujita,

    1. Department of Cytology & Histology, Okayama University Graduate School, Medicine, Dentistry and Pharmaceutical Sciences, Shikata, Okayama, Japan
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  • Kozo Utsumi,

    1. Department of Cytology & Histology, Okayama University Graduate School, Medicine, Dentistry and Pharmaceutical Sciences, Shikata, Okayama, Japan
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  • Junzo Sasaki

    1. Department of Cytology & Histology, Okayama University Graduate School, Medicine, Dentistry and Pharmaceutical Sciences, Shikata, Okayama, Japan
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Abstract

Membrane permeability transition (MPT) of mitochondria has an important role in apoptosis of various cells. The classic type of MPT is characterized by increased Ca2+ 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.

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