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+ 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.
Key wordsL-propionyl-carnitine mitochondrial membrane potential mitochondrial Ca2+ short-chain acyl-CoA long-chain acyl-CoA perfused rat heart ischemia
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