The growth of Plasmodium falciparum, a human malaria parasite, is sensitive to inhibition by chelators of several types. The alkylthiocarbamates and 8-hydroxyquinoline at pharmacologic doses selectively inhibit glycolysis within 6 hr in parasitized erythrocytes. The mechanism attributed to these agents is through the extracellular formation of lipid-soluble 2:1 metal complexes which enter susceptible cells and liberate a lethal 1:1 complex. This study further supports this mechanism since the uptake of 59Fe:oxine complexes within 6 hr occurs at doses corresponding to, or less than, those producing the lethal effects and metabolic changes. Fifty per cent of the uptake occurs in less than 6 hr. The presence of 8-hydroxyquinoline facilitates entry of the radiolabeled cations and uninfected erythrocytes take up less cation, especially in the absence of chelator. The siderochromes, rhodotorulic acid and mycobactin P, when mixed with 59Fe, result in an insignificant uptake, i.e., none of the former and only 12% of the latter penetrate the parasitized cells in 6 hr. Less than 25% of 59Fe:iodochlorhydroxyquin enters infected cells and 8% enters normal erythrocytes, suggesting that very little antimicrobial activity of the iodinated oxines is due to chelation unlike an agent such as KAN-322. In fact, 30% of the oxine complex and possibly more KAN-322 appears to partition in the intracellular parasite itself.