TY - JOUR
T1 - Palmitoleic acid induces the cardiac mitochondrial membrane permeability transition despite the presence of L-carnitine
AU - Oyanagi, Eri
AU - Uchida, Masataka
AU - Miyakawa, Takeshi
AU - Miyachi, Motohiko
AU - Yamaguchi, Hidetaka
AU - Nagami, Kuniatsu
AU - Utsumi, Kozo
AU - Yano, Hiromi
N1 - Funding Information:
We thank the staff of the Physiological-Function Center of Kawasaki Medical School. This work was supported by the Ryobi Teien Memory Foundation (to H.Y.), Okayama Medica (12-04; to H.Y), The Interdepartmental Research Fund of Kawasaki University of Medical Welfare (H24-08; to H.Y.), The Young Research Grant from JSPFSM in the Chugoku/Shikoku Region (12-007; to E.O.) and the Uesuko (to E.O.).
Publisher Copyright:
© 2015 Elsevier Inc. All rights reserved.
PY - 2015
Y1 - 2015
N2 - Although palmitoleic acid (C16:1) is associated with arrhythmias, and increases in an age-dependent matter, the effects of L-carnitine, which is essential for the transport of long-chain fatty acids into the mitochondria, are unclear. It has been postulated that L-carnitine may attenuate palmitate (C16:0)-induced mitochondrial dysfunction and the apoptosis of cardiomyocytes. The aim of this study was to elucidate the activity of L-carnitine in the prevention of the palmitoleic acid-induced mitochondrial membrane permeability transition and cytochrome c release using isolated cardiac mitochondria from rats. Palmitoleoyl-CoA-induced mitochondrial respiration was not accelerated by L-carnitine treatment, and this respiration was slightly inhibited by oligomycin, which is an inhibitor of ATP synthase. Despite pretreatment with L-carnitine, the mitochondrial membrane potential decreased and mitochondrial swelling was induced by palmitoleoyl-CoA. In the presence of a combination of L-carnitine and tiron, a free radical scavenger, there was attenuated mitochondrial swelling and cytochrome c release following palmitoleoyl-CoA treatment. We concluded that palmitoleic acid, but not palmitate, induces the cardiac mitochondrial membrane permeability transition despite the presence of L-carnitine.
AB - Although palmitoleic acid (C16:1) is associated with arrhythmias, and increases in an age-dependent matter, the effects of L-carnitine, which is essential for the transport of long-chain fatty acids into the mitochondria, are unclear. It has been postulated that L-carnitine may attenuate palmitate (C16:0)-induced mitochondrial dysfunction and the apoptosis of cardiomyocytes. The aim of this study was to elucidate the activity of L-carnitine in the prevention of the palmitoleic acid-induced mitochondrial membrane permeability transition and cytochrome c release using isolated cardiac mitochondria from rats. Palmitoleoyl-CoA-induced mitochondrial respiration was not accelerated by L-carnitine treatment, and this respiration was slightly inhibited by oligomycin, which is an inhibitor of ATP synthase. Despite pretreatment with L-carnitine, the mitochondrial membrane potential decreased and mitochondrial swelling was induced by palmitoleoyl-CoA. In the presence of a combination of L-carnitine and tiron, a free radical scavenger, there was attenuated mitochondrial swelling and cytochrome c release following palmitoleoyl-CoA treatment. We concluded that palmitoleic acid, but not palmitate, induces the cardiac mitochondrial membrane permeability transition despite the presence of L-carnitine.
KW - Cytochrome c
KW - Membrane potential
KW - Palmitoleoyl-CoA
KW - Palmitoyl-CoA
KW - Swelling
KW - Tiron
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U2 - 10.1016/j.bbrc.2015.05.011
DO - 10.1016/j.bbrc.2015.05.011
M3 - Article
C2 - 25983324
AN - SCOPUS:84934950780
SN - 0006-291X
VL - 463
SP - 29
EP - 36
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1-2
ER -