Abstract
The effects of the fatty acid ester palmitoyl carnitine (PC) on mitochondrial Ca 2+ handling and ATP synthesis are described. At low concentrations (5–40 μM) PC was found to produce changes in mitochondrial Ca 2+ handling, the most significant effect (P < 0.05) being the promotion of Ca 2+ efflux ( EC 25 = 1.19 ± 0.11 μ M) . Studies on mitochondrial substrate oxidation in the presence of either glutamate plus malate, or succinate, confirmed the ability of PC (10–100 μM) to cause loss of respiratory control as shown by reductions in the Respiratory Control Index for each substrate. It was concluded that the effect of PC on Ca 2+ transport was due to a direct action on the Na +Ca 2+ antiporter system, whilst the effect on respiration was due to an uncoupling action.
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