Abstract
The antimalarial specificity of chloroquine (CQ) stems from the saturable uptake of the drug into malaria parasites. Strains of Plasmodium falciparum that are resistant to CQ have evolved a mechanism to reduce the saturable uptake of CQ and several biochemical models have been proposed to explain this. These include an efflux process analogous to multi-drug resistance (MDR) in cancer cells, reduced proton trapping due to elevated vacuolar pH, reduced binding to an intracellular receptor and reduced activity of a permease or drug importer. Here, we attempt to reconcile many of the apparently conflicting data used to support these models. Previous data are analysed in the context of our own model in which CQ uptake is determined by access of the drug to ferriprotoporphyrin IX (FPIX), the intracellular receptor. Copyright 1999 Harcourt Publishers Ltd.
Published Version
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