Kaminsky R, Zweygarth E
International Laboratory for Research on Animal Diseases, ILRAD, Nairobi, Kenya.
Acta Trop. 1991 Aug;49(3):215-25. doi: 10.1016/0001-706x(91)90040-q.
Following previous studies of verapamil reversal of multidrug resistance in cancer cells and chloroquine resistance in malaria, the effect of the calcium channel blocker verapamil was investigated on multidrug-resistant and susceptible Trypanosoma brucei brucei. Resistance of cloned parasites to diminazene aceturate (Berenil) and isometamidium chloride (Samorin) was expressed in a cell-free in vitro culture system. Verapamil showed antitrypanosomal activity against both, multidrug-resistant and susceptible trypanosomes at concentrations above 1 micrograms/ml. Verapamil did not reverse multidrug resistance when used at concentrations of 0.1 or 1.0 micrograms/ml in combination with diminazene aceturate or isometamidium chloride. Results obtained in vitro correlate with observations in mice. It is suggested that multidrug resistance in African trypanosomes is due to mechanisms other than those occurring in cancer cells, malaria or South-American trypanosomiasis.
继之前对维拉帕米逆转癌细胞多药耐药性以及疟原虫氯喹耐药性的研究之后，研究了钙通道阻滞剂维拉帕米对多药耐药和敏感型布氏布氏锥虫的作用。在无细胞体外培养系统中表达了克隆寄生虫对乙酰氨基苯脒（贝尼尔）和氯甲脒（沙莫林）的耐药性。维拉帕米在浓度高于1微克/毫升时，对多药耐药和敏感型锥虫均显示出抗锥虫活性。当维拉帕米以0.1或1.0微克/毫升的浓度与乙酰氨基苯脒或氯甲脒联合使用时，并未逆转多药耐药性。体外获得的结果与在小鼠身上的观察结果相关。有人提出，非洲锥虫的多药耐药性是由不同于癌细胞、疟疾或南美锥虫病所出现的机制导致的。
