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Superoxide release is involved in membrane potential changes in mouse peritoneal macrophages
I A Gamaley1, K M Kirpichnikova, I V Klyubin
1Institute of Cytology, Russian Academy of Sciences, St. Petersburg. igamaley@link.cytspb.rssi.ru
Free Radical Biology & Medicine
|January 22, 1998
Summary
Reactive oxygen species (ROS) mediate macrophage hyperpolarization. Superoxide release, triggered by fMLP and PAF, influences membrane potential changes, dependent on calcium and potassium levels.
Area of Science:
- Immunology
- Cellular Physiology
Background:
- Macrophages play a crucial role in immune responses.
- Membrane potential changes are critical for macrophage function.
- Reactive oxygen species (ROS) are implicated in cellular signaling.
Purpose of the Study:
- To investigate the role of ROS in modulating macrophage membrane potential.
- To elucidate the mechanisms underlying membrane potential changes induced by various agonists.
Main Methods:
- Macrophage treatment with agonists (fMLP, PAF, LPS, IFN-γ).
- Measurement of membrane potential using electrophysiological techniques.
- Chemiluminescence assays to detect ROS production.
- Pharmacological inhibition of ROS and ion channels.
Main Results:
- fMLP and PAF induced depolarization followed by hyperpolarization, associated with ROS release.
- LPS and IFN-γ caused only depolarization.
- Superoxide dismutase, but not catalase, reduced hyperpolarization.
- A xanthine/xanthine oxidase system mimicked hyperpolarization.
- Hyperpolarization was dependent on intracellular Ca2+ and extracellular K+.
- Quinidine blocked Ca2+-dependent K+ channels, altering depolarization and reducing ROS effects.
Conclusions:
- Macrophage hyperpolarization induced by fMLP and PAF is mediated by superoxide.
- This process involves a Ca2+-dependent alteration in K+ permeability.
- ROS play a significant role in regulating macrophage membrane potential and function.