Concurrent inhibition by tunicamycin of glycosylation and parasitemia in malarial parasites (Plasmodium falciparum) cultured in human erythrocytes.

Tunicamycin (0.1--10 microgram/ml) incubated 96 h with human erythrocytes infected with malarial parasites significantly decreased parasitemia compared to controls. The antimalarial effect of tunicamycin was dose-related and paralleled its inhibition of the incorporation of radiolabeled glucosamine into parasite-derived membrane macromolecules. Tunicamycin had no significant effect on isoleucine incorporation into parasite-derived macromolecules. These results suggest that tunicamycin may act by inhibition of the glycosylation of parasite macromolecules. The results also indicate the role of glycosylated macromolecules in the survival of the erythrocytic stage of Plasmodium falciparum and the potential for selective inhibitors of the glycosylation of parasite macromolecules as agents for malarial chemotherapy.