Protective mechanism of .BETA.-cyclodextrin for the hemolysis induced with phenothiazine neuroleptics in vitro.

Abstract

.beta.-Cyclodextrin (.beta.-CyD) protected the human erythrocytes from the hemolysis induced with 10 phenothiazine neuroleptics [promazine, methoxypromazine, chlorpromazine, promethazine, trimeprazine, perazine, prochlorperazine, trifluoperazine, perphenazine and fluphenazine] in isotonic solution. The hemolytic activities of the phenothiazine-.beta.-CyD systems appeared to depend upon the free phenothiazine concentration, suggesting that the complexed form of phenothiazines is essentially inactive to cause hemolysis. The binding abilities and surface activities of the complexed form of phenothiazines were much smaller than those of free phenothiazines. The protective effect of .beta.-CyD may be due to the decrease in the effective hemolytic concentration of phenothiazines by inclusion complexation rather than the stabilizing effect of .beta.-CyD on the erythrocyte membrane.