Transport of carbohydrates by malarial parasites

Bulletin of the World Health Organization, 55 (2-3): 227 (1977) Transport of carbohydrates by malarial parasites C. A. HOMEWOOD 1 The red cells of malaria-infected mice and ducks have an increased permeability to glucose. In spite of the necessity for the intraerythrocytic stages of malarial parasites to obtain large quantities of glucose, surprisingly little is known of the mechanism by which the sugar reaches the parasite, or even which sugars can be used. Early experi- ments on the utilization of carbohydrates by parasites or parasitized erythrocytes relied on a change in the respiration of the cells to indicate consumption of the sugar (1, 2), and as discussed in the following paper of this issue, the results of this test are likely to be misleading. As remarked by Herman et al. (3), intraerythro- cytic Plasmodium lophurae would be unable to use glucose at the observed rate unless it had increased the low permeability of the duck erythrocyte. The same must be true of P. berghei in the mouse, but may not apply to malarial parasites of humans, whose normal erythrocytes are readily permeable to glucose. Sherman & Tanigoshi (4) showed that P. lophurae 1 Lecturer, Department of Parasitology, Liverpool School of Tropical Medicine, Pembroke Place, Liverpool L3 5QA, England. does indeed change the permeability of the duck erythrocyte so that glucose enters it more rapidly. The increased rate of entry is due to an increase in diffusion rather than in carrier-mediated transport. Diffusion of glucose into mouse red cells containing P. berghei is also increased, as shown by the entry of L-glucose into parasitized cells but not into normal cells (5, 6). The phenomenon of increased rate of diffusion of glucose into parasitized cells may be a general consequence of intraerythrocytic parasitism, as it has been observed also for red cells from mice infected with Anthemosoma garnhami (7) or with Babesia rodhaini (8). The mechanism by which the permeability of the membranes of the host cell is changed is not known, but with P. berghei it occurs only in those cells that contain parasites (5). The parasite must therefore exert a direct action on the membrane, and it would be expected that any sub- stance able to inhibit this action would be an effective antimalarial agent. Whether it would also act against the primate malarias cannot at the moment be pre- dicted. RtSUM1 TRANSPORT DES GLUCIDES PAR LES PARASITES DU PALUDISME On a montre que l'infection des erythrocytes de canard par Plasmodium lophurae augmentait leur per- meabilite, permettant ainsi une penetration plus rapide du glucose. L'accroissement de sa vitesse d'entree est du a une meilleure diffusion plut6t qu'A un transport plus actif par le porteur. La diffusion du glucose dans les erythrocytes de souris infectes par P. berghei est egale- ment augmentee, comme l'indique l'entree de L-glucose dans les cellules parasitees et non dans les cellules normales. REFERENCES 1. FULTON, J. D. Annals oftropical medicine andparasito- logy, 33: 217-227 (1939). 2. MAIER, J. & COGGESHALL, L. T. Journal of infectious diseases, 69: 87-96 (1941). 3. HERMAN, Y. F. ET AL. American journal of tropical medicine and hygiene, 15: 276-280 (1966). 4. SHERMAN, I. W. & TANIGOSHI, L. Journal of proto- zoology, 21: 603-607 (1974). 5. NEAME, K. D. & HOMEWOOD, C. A. International journalfor parasitology, 5: 537-540 (1975). 6. HOMEWOOD, C. A. & NEAME, K. D. Nature, 252: 718- 719 (1974). 7. MOMEN, H. ET AL. Annals of tropical medicine and parasitology, 69: 512-520 (1975). 8. HOMEWOOD, C. A. ET AL. Annals of tropical medicine andparasitology, 69: 429-434 (1975). 3600 227-