Water and urea transport in human erythrocytes infected with the malaria parasite Plasmodium falciparum.

The permeability properties of the human red cell membrane to various solutes are altered by malarial infection. In the present work we show that the permeability of the red cell membrane to water is also affected by the intraerythrocytic growth of the malaria parasite Plasmodium falciparum, whereas urea permeability appears unchanged. The data from infected cells show decreases in membrane surface area, cell volume, the osmotically active water fraction (Weff), and osmotic water permeability (Pf) as measured by stopped-flow spectroscopy. On the other hand, the data suggest an increase in diffusive water permeability (Pd) in infected cells with no change in urea permeability when measured by the continuous flow method. The decreased Pf/Pd ratio of infected cell membranes and its implications in the geometry of the red cell membrane water channel or pore are discussed.

[1]  I. Sherman,et al.  Biochemistry of Plasmodium (malarial parasites). , 1979, Microbiological reviews.

[2]  H. Ginsburg,et al.  New permeability pathways induced in membranes of Plasmodium falciparum infected erythrocytes. , 1983, Molecular and biochemical parasitology.

[3]  C. Lambros,et al.  Synchronization of Plasmodium falciparum erythrocytic stages in culture. , 1979, The Journal of parasitology.

[4]  G. Mitchell.  The Wellcome Trust Lecture , 1989, Parasitology.

[5]  H. Ginsburg,et al.  Uptake of L-tryptophan by erythrocytes infected with malaria parasites (Plasmodium falciparum). , 1983, Biochimica et biophysica acta.

[6]  D. Levitt,et al.  Urea and ethylene glycol-facilitated transport systems in the human red cell membrane. Saturation, competition, and asymmetry , 1983, The Journal of general physiology.

[7]  I. Sherman,et al.  Incorporation of 14C-amino acids by malarial plasmodia (Plasmodium iophurae). VI. Changes in the kinetic constants of amino acid transport during infection. , 1974, Experimental parasitology.

[8]  Victor W. Sidel,et al.  Osmotic Properties of Human Red Cells , 1964, The Journal of general physiology.

[9]  A. K. Solomon,et al.  THE AQUEOUS PORE IN THE RED CELL MEMBRANE: BAND 3 AS A CHANNEL FOR ANIONS, CATIONS, NONELECTROLYTES, AND WATER * , 1983, Annals of the New York Academy of Sciences.

[10]  D. Tosteson,et al.  Effects of bicarbonate on lithium transport in human red cells , 1978, The Journal of general physiology.

[11]  J. Brahm.  Diffusional water permeability of human erythrocytes and their ghosts , 1982, The Journal of general physiology.

[12]  D. Levitt,et al.  Reflection coefficient and permeability of urea and ethylene glycol in the human red cell membrane , 1983, The Journal of general physiology.

[13]  J. Brahm.  Temperature-dependent changes of chloride transport kinetics in human red cells , 1977, The Journal of General Physiology.

[14]  R. S. Haber,et al.  The concentration dependence of active K+ transport in the turkey erythrocyte. Hill analysis and evidence for positive cooperativity between ion binding sites , 1983, The Journal of general physiology.

[15]  H. Ginsburg,et al.  Permselectivity changes in malaria (Plasmodium falciparum) infected human red blood cell membranes , 1983, Journal of cellular physiology.

[16]  A. K. Solomon,et al.  ENTRANCE OF WATER INTO HUMAN RED CELLS UNDER AN OSMOTIC PRESSURE GRADIENT , 1957, The Journal of general physiology.

[17]  I. Sherman.  Membrane structure and function of malaria parasites and the infected erythrocyte , 1985, Parasitology.

[18]  R. Macey.  Transport of water and urea in red blood cells. , 1984, The American journal of physiology.

[19]  Jensen Wn,et al.  A direct method for the quantitative measurement of red cell dimensions. , 1961 .

[20]  W. Galey,et al.  The failure of hydrodynamic analysis to define pore size in cell membranes. , 1985, Biochimica et biophysica acta.

[21]  R. Wilson,et al.  Separation of viable schizont-infected red cells of Plasmodium falciparum from human blood. , 1978, Annals of tropical medicine and parasitology.

[22]  A. K. Solomon,et al.  THE RATE OF EXCHANGE OF TRITIATED WATER ACROSS THE HUMAN RED CELL MEMBRANE , 1957, The Journal of general physiology.

[23]  H. Ginsburg,et al.  Alterations in membrane permeability of malaria-infected human erythrocytes are related to the growth stage of the parasite. , 1982, Biochimica et biophysica acta.

[24]  R. Mikkelsen,et al.  Preoperative inferior vena cava filter implantation to prevent pulmonary fat embolism in a patient showing renal angiomyolipoma extension into the renal vein: A case report and literature review , 2018, Journal of rural medicine : JRM.

[25]  J. Brahm.  Urea permeability of human red cells , 1983, The Journal of general physiology.

[26]  I. Sherman,et al.  Glucose transport in the malarial (Plasmodium lophurae) infected erythrocyte. , 1974, The Journal of protozoology.

[27]  W. Trager,et al.  Human malaria parasites in continuous culture. , 1976, Science.

[28]  W. Hager.  Dual techniques for constrained optimization , 1987 .

[29]  P. Lacelle.  Effect of sphering on erythrocyte deformability. , 1972, Biorheology.

[30]  I. W. Sherman.  Transport of amino acids and nucleic acid precursors in malarial parasites. , 1977, Bulletin of the World Health Organization.

[31]  H. Ginsburg,et al.  New permeability pathways induced by the malarial parasite in the membrane of its host erythrocyte: Potential routes for targeting of drugs into infected cells , 1987, Bioscience reports.

[32]  R. Macey,et al.  Properties of water channels in human red cells. , 1972, Biomembranes.

[33]  A. K. Solomon.  Characterization of Biological Membranes by Equivalent Pores , 1968, The Journal of general physiology.

[34]  E. M. Renkin,et al.  FILTRATION, DIFFUSION, AND MOLECULAR SIEVING THROUGH POROUS CELLULOSE MEMBRANES , 1954, The Journal of general physiology.

[35]  A. Finkelstein,et al.  Water permeability of gramicidin A-treated lipid bilayer membranes , 1978, The Journal of general physiology.

[36]  H. Ginsburg,et al.  Characterization of permeation pathways appearing in the host membrane of Plasmodium falciparum infected red blood cells. , 1985, Molecular and biochemical parasitology.