Glucose Transport in the Malarial (Plasmodium lophurae) Infected Erythrocyte*

Abstract

SYNOPSIS Plasmodium lophurae‐infected red blood cells utilized considerably greater quantities of glucose than did uninfected duckling red cells. Kinetic analysis of glucose transport showed: (A). Below a concentration of 2 mM in the medium the uptake process followed Michaelis‐Menten kinetics (carrier‐mediated facilitated diffusion) whereas at concentrations greater than this simple diffusion became the main mode of entry. (B). The apparent transport constants, Kt, for normal and infected cells were similar. However there was an 8‐fold increase in the maximal velocity, Vmax, for infected cells. (C). “Free” malaria parasites had a significantly lower Kt and a higher Vmax than did normal or infected red cells. Entry and exit studies with the nonmetabolizable sugar analog, 3‐0‐methyl glucose, demonstrated that the enhanced rate of uptake by infected cells involved an increase in the simple diffusion component and the degree of enhancement was correlated with the size of the intracellular parasite. Competition experiments suggested that in the malaria‐infected cell one locus is involved in the carrier‐mediated transport of glucose, mannose and galactose whereas another locus transports fructose and/or glycerol. These results indicate that the enhanced entry of glucose into the malaria‐infected red cell is a consequence of factors other than increased glucose catabolism by the host‐parasite complex, and the host cell's capacity to take up greater quantities of sugar directly involves the growing intracellular plasmodium.

Malaria parasite Plasmodium gallinaceum up‐regulates host red blood cell channels

“…Malaria‐infected human and avian RBCs also show increased transport of a variety of non‐electrolytes [5,7]. There is also good evidence for enhanced sorbitol and taurine uptake into malaria‐infected chicken RBCs under physiological conditions via a malaria‐induced pathway [23].…”

“…New permeation pathways (NPP) exist in human [5] and murine malaria‐infected RBCs [6] and a reanalysis of earlier work [7] suggests their presence in malaria‐infected avian RBCs. Kirk and co‐workers [5] reported that the NPP in malaria‐infected human RBCs are broad‐specificity pathways of a single type, which show the characteristics of an anion channel.…”

Biophysical analysis of novel transport pathways induced in red blood cell membranes

“…Such is the case for the myo-inositol required for the synthesis of phosphatidylinositol (Vial, Thuet & Philippot, 1982), for lactate which is the main waste product of the energy metabolism of the infected cell (Pfaller et al, 1982) and for several amino acids which the parasite has to import from the extracellular space (Sherman, 1979). One was, therefore, not surprised to find that the membrane of the infected cell is highly permeable to amino acids (Sherman & Tanigoshi, 1974b), hexoses (Homewood & Neame, 1974;Sherman & Tanigoshi, 1974a), myo-inositol (Elford et al, 1985) and polyols (Lambros & Vanderberg, 1979). Recently, a thorough survey has been performed of the permeability pattern of human erythrocytes, infected with Plasmodium falciparum to anions, carbohydrates and amino acids (Kutner, Ginsburg & Cabantchik, o.5, 1983;Ginsburg et al, 1983Ginsburg et al, , 1985.…”

Comparative biology of intracellular parasitism.

“…Erythrocytes parasitized with P. berghei and P. lophurae actually catabolize glucose at rates exceeding its rate of entry into unparasitized host cells. The plasmodia have solved this dilemma by bringing about an increase in the rate at which glucose enters the parasitized erythrocyte (299,371). The related blooddwelling Babesia rodhaini brings about a similar change in its mouse erythrocyte host (195).…”