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Naloxone inhibits superoxide release from human neutrophils

Discussion in ''Conditions related to ME/CFS' news and research' started by Mister Person, Feb 3, 2023.

  1. Mister Person

    Mister Person Established Member (Voting Rights)

    Messages:
    77
    Perhaps this is another mechanism for LDN? I don't understand. Younger mentioned nadph oxidase, astrocytes, opiod growth factor, and the rebound endorphin. But no mention of this neutrophil paper
     
    Mister Person, Feb 3, 2023
    #1
    Peter Trewhitt likes this.
  2. Trish

    Trish Moderator Staff Member

    Messages:
    52,218
    Location:
    UK
    I assume you are referring to this paper from 1985:
    Naloxone inhibits superoxide release from human neutrophils
    Simpkins et al.
    Abstract
    Using the superoxide dismutase inhibitable reduction of cytochrome c assay, we studied, the effect of (-) naloxone on N-formyl-methionyl-leucyl-phenylalanine (FMLP) stimulated superoxide (O2-) release from human neutrophils. Neutrophils were pre-incubated with the range of concentrations of (-) naloxone that is administered in models of experimental sepsis (10(-6) - 10(-4.5) M). (-) Naloxone inhibited O2- release in a dose dependent manner. 02- produced by a cell-free xanthine-xanthine oxidase system was not inhibited by (-) naloxone, indicating that (-) naloxone was not scavanging O2-. There was no difference between the effect of (-) and (+) naloxone suggesting that the inhibition of O2- was not specific for an opiate receptor. Another opiate antagonist, nalorphine, as well as the opiate agonist, morphine, also inhibited O2- release in the same concentration range. There was no difference between the effect of naloxone and morphine.
    ____________________

    Note that LDN is Low Dose Naltrexone, not naloxone.

    From     WebMD
     
    Trish, Feb 3, 2023
    #2
    alktipping and Peter Trewhitt like this.

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