Abstract
Ethanol stimulates the Na +-dependent Ca 2+ efflux in brain mitochondria and inhibits the Na +-independent Ca 2+-efflux [12]. Here, we studied the effects of n-alkanols on the various Ca 2+ transport processes in brain mitochondria. Only short-chain alcohols (i.e. methanol, ethanol and propanol) stimulated Na + Ca 2+ exchange. The inhibition of H + Ca 2+ exchange was significant only with ethanol. Short-chain alcohols inhibit while long-chain alcohols activate the cyclosporin-sensitive Ca 2+-efflux. These data suggest that the mechanism of the alkanols' effects on Na + Ca 2+ exchange, H + Ca 2+ exchange and the cyclosporin sensitive pore are entirely different. Alkanols have no effect on the electrogenic Ca 2+ uniporter. Ethanol did not affect the apparent K 0.5 for Na + (7.5 mM) of the Na + Ca 2+ exchange. Similarly, the magnitude of the effect of ethanol did not depend on matrix Ca 2+ concentration, suggesting that short-chain alkanols do not stimulate the rate of Na + Ca 2+ exchange by increasing the affinity of the carrier to Ca 2+ in or Na + out. High concentrations of K +, Mg 2+ and Ca 2+ enhanced the ethanol effect. It is possible that high surface potential attenuates the effect of ethanol. It is suggested that ethanol stimulation of Na + Ca 2+ exchange depends on the modulation of the surface dielectric constant.
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