Abstract
IN a previous communication1 it was reported, that the antimalarial drug, chloroquine, becomes highly concentrated in red blood cells containing the malarial parasite, Plasmodium berghei, through a mechanism of uptake which appears qualitatively distinct from that of uninfected red blood cells, plasma and host tissues. It was suggested that the ability of chloroquine to become selectively concentrated in the infected red cell constitutes the essential basis of its antimalarial activity. Because red blood cells parasitized by a strain of P. berghei resistant to chloroquine absorbed less than half the amount taken up by erythrocytes infected with the chloroquine-sensitive parent strain, the phenomenon of selective drug uptake may in part account for drug resistance. We report here observations on the sequential morphological changes produced by chloroquine in P. berghei in mice. Use of the same experimental model allows us to correlate changes in the structure of the parasite with changes in drug concentration in the parasitized red cell and suggests a mechanism by which the drug becomes concentrated in the parasite.
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