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Myocrisin-mediated oxidative stress

J Reglinski1, D E Paterson, S Latimer

  • 1Department of Pure and Applied Chemistry, Strathclyde University, Glasgow, UK. j.reglinski@strath.ac.uk

Clinica Chimica Acta; International Journal of Clinical Chemistry
|March 12, 1998
PubMed
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Myocrisin treatment in rheumatoid arthritis patients increases monocyte hydrogen peroxide production and reduced glutathione levels. This gold therapy appears to elevate oxidative stress in vivo.

Area of Science:

  • Biochemistry
  • Immunology
  • Pharmacology

Background:

  • Rheumatoid arthritis (RA) involves complex immune responses and oxidative stress.
  • Gold compounds, like myocrisin, have been used to treat RA, but their cellular mechanisms are not fully understood.
  • Monocytes play a key role in RA pathogenesis and oxidant production.

Purpose of the Study:

  • To investigate the effect of myocrisin on oxidant production and detoxification in monocytes.
  • To examine the impact of myocrisin on glutathione metabolism in monocytes.
  • To determine if myocrisin influences oxidative stress in vivo.

Main Methods:

  • Monocytes were isolated from rheumatoid arthritis patients treated with myocrisin, patients on NSAIDs, and healthy volunteers.
  • Hydrogen peroxide production by monocytes was measured.

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  • Levels of reduced glutathione (GSH) and oxidized glutathione (GSSG) in monocytes were quantified.
  • Glutathione reductase and glutathione peroxidase activities were assessed.

    • Main Results:

    • Monocytes from myocrisin-treated RA patients produced significantly higher levels of hydrogen peroxide (14.9 nmoles/10(6) cells) compared to NSAID-treated patients (11.3 nmoles/10(6) cells) and healthy volunteers (11.2 nmoles/10(6) cells).
    • Myocrisin-treated patients showed elevated monocyte reduced glutathione (GSH) levels (2.4 mmol/l) and depressed diglutathione (GSSG) levels (0.97 micromol/l) compared to healthy volunteers (GSH: 0.83 mmol/l; GSSG: 5.71 micromol/l).
    • Gold therapy did not inhibit glutathione reductase but did inhibit glutathione peroxidase.

    Conclusions:

    • Myocrisin appears to increase monocyte hydrogen peroxide production and reduce glutathione levels in vivo.
    • The observed changes in glutathione metabolism, coupled with inhibited glutathione peroxidase activity, suggest that myocrisin contributes to increased oxidative stress in monocytes.
    • These findings provide insight into the cellular mechanisms of gold therapy in rheumatoid arthritis.