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Transport processes of 2-deoxy-D-glucose in erythrocytes infected with Plasmodium yoelii, a rodent malaria parasite

Published online by Cambridge University Press:  06 April 2009

A. Izumo
Affiliation:
Department of Medical Zoology, Osaka City University Medical School, Asahi-machi, Abeno-ku, Osaka 545, Japan
K. Tanabe
Affiliation:
Department of Medical Zoology, Osaka City University Medical School, Asahi-machi, Abeno-ku, Osaka 545, Japan
M. Kato
Affiliation:
Department of Medical Zoology, Osaka City University Medical School, Asahi-machi, Abeno-ku, Osaka 545, Japan
S. Doi
Affiliation:
Department of Legal Medicine, Kinki University School of Medicine, Osaka-Sayama, Osaka 589, Japan
K. Maekawa
Affiliation:
Department of Medical Zoology, Osaka City University Medical School, Asahi-machi, Abeno-ku, Osaka 545, Japan
S. Takada
Affiliation:
Department of Medical Zoology, Osaka City University Medical School, Asahi-machi, Abeno-ku, Osaka 545, Japan

Summary

The transport processes of D-glucose in Plasmodium yoelii-infected mouse erythrocytes were investigated using 2-deoxy-D-glucose (2DOG), a non-metabolizable analogue of D-glucose. Infected cells showed an increase in the uptake of 2DOG compared to uninfected controls, and an effect which was more prominent in cells with mature-stage parasites. Kinetic studies measuring the initial rates of 2DOG uptake revealed two components in infected cells with late trophozoite and schizont-stage parasites: a simple diffusion system and a carrier (transporter)-mediated system. The transporter was common for D-glucose and 2DOG and had a kinetic constant indicating a high affinity for 2DOG (the Km = 0·18 mM and the Vmax = 0·61 mmol/1010 cells/min), as compared to the constant of the mouse erythrocyte carrier (the Km = 10 mM and the Vmax = 1·8 mmol/1010 cells/min). Determination of the distribution of [3H]2DOG in infected cells and experiments with metabolic inhibitors indicated that the simple diffusion system localizes in the membrane of host cells and the transporter in the parasite plasma membrane. The parasite glucose transporter was much less sensitive to cytochalasin B than that of the host cells and the uptake of 2DOG via the transporter was dependent on energy. Based on these findings, the following features emerge: D-glucose first gains access to the cytosol of infected erythrocytes via the simple diffusion system, which appears after infection by the parasite, and an active uptake against the concentration gradient takes place at the parasite plasma membrane via the parasite glucose transporter in an energy dependent manner. Finally, an energy transduction mechanism for the transport of glucose across the parasite plasma membrane is discussed.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1989

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