Abstract

1-Palmitoylcarnitine (1-PC) reduced the electrophoretic mobility of human erythrocytes bathed in low ionic strength solution. Unlike divalent cations which appear to reduce electrophoretic mobility by screening surface negative charge, cationic 1-PC does so by being incorporated into the plasma membrane. Incorporation of 1-PG was assessed directly by measurement of the partition coefficients which are 1.18 × 10 5 and 1.38 × 10 5 in sarcoplasmic reticulum vesicles and erythrocyte ghosts, respectively. The hydrophobic nature of the amphiphile interaction with erythrocyte membrane was also evident as an antihemolytic effect at 1-PC concentrations that also reduced electrophoretic mobility. Moreover, the potency and efficacy of acylcarnitines to reduce electrophoretic mobility increased as the acyl chain length increased. 1-PC also reduced the electrophoretic mobility of guinea-pig ventricular myocytes in low ionic strength solution. Estimation of the zeta potential yielded positive shifts of 4mV in myocytes and 5mV on crythrocytes at 1 μM 1-PC. These voltage shifts are essentially the same as those reported for activation and inactivation of sodium and calcium currents in myocytes. Therefore, the surface charge effect of 1-PC depends upon membrane incorporation and underlies the electrophysiological actions of the amphiphile including arrhythmias.

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