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Decrease of transport of some polyols in sickle cells.

C T Craescu, R Cassoly, F Galacteros

    Biochimica Et Biophysica Acta
    |September 5, 1984
    PubMed
    Summary
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    Sickle cells show reduced transport of ethylene glycol and glycerol compared to normal red blood cells, indicating membrane protein changes. Erythritol transport remains unaffected, suggesting specific alterations in sickle cell membranes.

    Area of Science:

    • Biophysics
    • Cell Biology
    • Hematology

    Background:

    • Sickle cell disease involves altered red blood cell properties.
    • Erythrocyte membrane transport is crucial for cell function.
    • Small non-electrolyte transport kinetics in sickle cells are not fully understood.

    Purpose of the Study:

    • To investigate the inward net-flux of small non-electrolytes in sickle cells versus normal erythrocytes.
    • To determine if sickle cell membranes exhibit altered permeability to specific non-electrolytes.

    Main Methods:

    • Kinetic studies using turbidimetric measurements for ethylene glycol and glycerol.
    • Hematocrit monitoring for erythritol transport rate evaluation.
    • Analysis of permeability coefficients under varying conditions (temperature, pH, oxygenation).

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    Main Results:

    • Sickle cells exhibited a 2-fold reduction in ethylene glycol permeability and a 4-fold reduction in glycerol permeability compared to normal erythrocytes.
    • No significant changes in erythritol transport kinetics were observed between sickle cells and normal erythrocytes.
    • Glycerol permeability dependence on temperature, pH, and oxygenation was similar in both cell types, but correlated with cell density only in sickle cells.

    Conclusions:

    • Irreversible modifications of membrane proteins involved in glycerol and ethylene glycol transport occur in sickle cells.
    • These findings suggest specific alterations in the erythrocyte membrane structure and function in sickle cell disease.
    • The differential transport kinetics highlight potential targets for understanding sickle cell pathophysiology.