TRYPTOPHAN-N-FORMYLATED GRAMICIDIN CAUSES GROWTH-INHIBITION OF PLASMODIUM-FALCIPARUM BY INDUCING POTASSIUM EFFLUX FROM INFECTED ERYTHROCYTES

In a study of the supposed selective action of tryptophan-N-formylated gramicidin (NFG) on infected erythrocytes as well as the relationship between the ability of NFG to inhibit parasite growth and its capacit y to induce potassium leakage from infected cells, a series of experim ents was performed in which in vitro cultures of Plasmodium falciparum were incubated with NFG or gramicidin. Those cultures were subsequent ly assayed for intracellular sodium and potassium contents, cell lysis , and/or parasite viability. It is shown and discussed that although N FG can attack both infected and uninfected erythrocytes, resulting in potassium efflux from and sodium influx into these cells, the effects are much greater on infected erythrocytes than on uninfected ones. Fur thermore, the results strongly suggest that NFG-mediated potassium eff lux is the direct cause of parasite death.