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[Glucose transport inhibition in human erythrocytes by calmodulin antagonists]

M I Kosovskiĭ, A I Gagel'gans

    Tsitologiia
    |September 1, 1986
    PubMed

    Insights

    Calmodulin antagonists block glucose transport in human red blood cells by affecting the carrier-sugar complex. Calcium ionophores reverse this inhibition, suggesting a calmodulin-dependent mechanism.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Pharmacology

    Context:

    • Glucose transport is crucial for erythrocyte energy metabolism.
    • Calmodulin is a key calcium-binding protein involved in cellular signaling.
    • Erythrocytes lack mitochondria and rely solely on glycolysis for ATP production.

    Purpose:

    • To investigate the effect of calmodulin antagonists on glucose transport in human erythrocytes.
    • To elucidate the mechanism underlying the inhibition of glucose transport by these antagonists.
    • To explore the role of calcium ions and calmodulin in regulating glucose transport.

    Summary:

    • Calmodulin antagonists (tryphtazin, lidocaine, dykain, palmitate) were found to inhibit glucose transport in human erythrocytes.
    • The inhibition was concentration-dependent and uncompetitive, decreasing the maximum transport rate but not the dissociation constant of the carrier-sugar complex.
    • Calcium ionophores (A23187, divaleryldibenzo-18-crown-6) abolished the inhibitory effects, indicating a calmodulin-dependent pathway.

    Impact:

    • Suggests a novel regulatory mechanism for glucose transport in erythrocytes involving calmodulin.
    • Provides insights into the potential therapeutic targets for modulating glucose metabolism.
    • Highlights the interplay between calcium signaling and carbohydrate transport.

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