Abstract
The imidazole antimycotics, miconazole, econazole and triclomazole as well as α-naphtoflavone, known as powerful inhibitors of cytochrome P 450 and previously recognized as K + channel blockers are shown to be potent activators of the base exchange enzyme system responsible for the biosynthesis of phosphatidylserine in Jurkat T cells. The inhibition of CD3-induced Ca 2+ influx by antimycotics but not by K + channel blockers, demonstrated that the rise in phosphatidylserine synthesis caused by the two classes of drugs, was independent of Ca 2+ influx in the cells. In addition, we show that the action of these drugs on phosphatidylserine synthesis was not mimicked by modifications of membrane potential. The regulation of both K + channels and the base exchange enzyme system thus occurs through a similar (or common) pathway that is independent of Ca 2+-influx and membrane potential.
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