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Hyperoxia reduces plasma membrane fluidity: a mechanism for endothelial cell dysfunction.

E R Block, J M Patel, K J Angelides

    Journal of Applied Physiology (Bethesda, Md. : 1985)
    |March 1, 1986
    PubMed
    Summary

    High oxygen levels (hyperoxia) reduce serotonin uptake in endothelial cells by decreasing plasma membrane fluidity. This study found no impact on Na+-K+-ATPase activity or ATP content, suggesting fluidity is key to altered cell function.

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    Area of Science:

    • Cell Biology
    • Physiology
    • Biochemistry

    Background:

    • Endothelial cells play a crucial role in regulating vascular function.
    • Hyperoxia, or high oxygen levels, has been observed to impair endothelial cell function, including serotonin uptake.
    • The precise mechanisms underlying hyperoxia-induced alterations in endothelial cell function require further elucidation.

    Purpose of the Study:

    • To investigate the mechanisms by which hyperoxia decreases serotonin uptake by endothelial cells.
    • To evaluate the roles of Na+-K+-ATPase activity, ATP content, and plasma membrane fluidity in this process.

    Main Methods:

    • Cultured pulmonary artery and aortic endothelial cells were exposed to hyperoxia (95% O2) or control conditions (20% O2).
    • Measurements included Na+-K+-ATPase activity, intracellular ATP content, and plasma membrane fluidity.

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  • These parameters were assessed over a time course of 4-42 hours.

    • Main Results:

    • Hyperoxia did not significantly affect Na+-K+-ATPase activity or ATP content in endothelial cells.
    • Hyperoxia led to a decrease in the fluidity of the endothelial cell plasma membrane.
    • The reduction in plasma membrane fluidity correlated with the inhibition of serotonin transport under hyperoxic conditions.

    Conclusions:

    • Hyperoxia-induced decreases in endothelial cell serotonin transport are primarily linked to reduced plasma membrane fluidity.
    • Alterations in the hydrophobic core of the plasma membrane may underlie functional impairments observed during hyperoxia.
    • These findings highlight the importance of membrane fluidity in endothelial cell response to oxygen levels.