Abstract
Treatment of normal mouse erythrocytes with a nonspecific protease from streptomyces griseus activates a saturable process for chloroquine accumulation. The apparent dissociation constant for the interaction of chloroquine with the saturable component of this latent process is 50 nM. This value is similar to that of a high-affinity process of chloroquine accumulation which hitherto has been observed only in erythrocytes infected with malaria parasites. In addition, the capacity of the latent process, approximately 30 μmoles per Kg of erythrocytes, is sufficient to account for the accumulation of chloroquine by erythrocytes infected with malaria parasites. These findings demonstrate the plausibility of attributing the ability to accumulate chloroquine with high affinity to the erythrocyte host rather than to the parasite.
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