L-propionyl-carnitine protection of mitochondria in ischemic rat hearts

The energy-linked processes (transmembrane potential and oxidative phosphorylation) resulted in impaired mitochondria isolated from ischemic perfused rat hearts. Addition of 1.5 mM L-propionyl-carnitine to the perfusate significantly reduced the ischemic damage and ameliorated mitochondrial Ca2+ hom...

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Veröffentlicht in:Molecular and cellular biochemistry 1989-06, Vol.88 (1-2), p.169-173
Hauptverfasser: Di Lisa, F, Menabò, R, Siliprandi, N
Format: Artikel
Sprache:eng
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Zusammenfassung:The energy-linked processes (transmembrane potential and oxidative phosphorylation) resulted in impaired mitochondria isolated from ischemic perfused rat hearts. Addition of 1.5 mM L-propionyl-carnitine to the perfusate significantly reduced the ischemic damage and ameliorated mitochondrial Ca2+ homeostasis. In both normoxic and ischemic hearts perfused with L-propionyl-carnitine a consistent amount of propionyl-CoA-otherwise undetectable-was produced. L-propionyl-carnitine treatment also prevented the decrease of succinyl-CoA associated with the ischemic condition. These results and the decrease of myocardial acetyl-CoA induced by exogenous L-propionyl-carnitine points to the anaplerotic effect of this ester. The consequently improved flux in the tricarboxylic-acid cycle may account for the observed protection of mitochondrial functions afforded by L-propionyl-carnitine in the ischemic perfused hearts.
ISSN:0300-8177
1573-4919
DOI:10.1007/BF00223439