Differences in trans-stimulated chloroquine efflux kinetics are linked to PfCRT in Plasmodium falciparum.

ABSTRACT: The mechanism underpinning chloroquine drug resistance in the human malarial parasite Plasmodium falciparum has remained controversial. Currently discussed models include a carrier or a channel for chloroquine, the former actively expelling the drug, the latter facilitating its passive diffusion, out of the parasite's food vacuole, where chloroquine accumulates and inhibits haem detoxification. Here we have challenged both models using an established trans-stimulation efflux protocol. While carriers may demonstrate trans-stimulation, channels do not. Our data reveal that extracellular chloroquine stimulates chloroquine efflux in the presence and absence of metabolic energy in both chloroquine-sensitive and -resistant parasites, resulting in a hyperbolic increase in the apparent initial eff

SUBMITTER: Sanchez CP 

PROVIDER: S-EPMC2944662 | biostudies-literature | 2007 Apr

REPOSITORIES: biostudies-literature