MYOCRISIN-MEDIATED OXIDATIVE STRESS

Citation
J. Reglinski et al., MYOCRISIN-MEDIATED OXIDATIVE STRESS, Clinica chimica acta, 268(1-2), 1997, pp. 85-99
Citations number
32
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Medical Laboratory Technology",Biology
Journal title
ISSN journal
0009-8981
Volume
268
Issue
1-2
Year of publication
1997
Pages
85 - 99
Database
ISI
SICI code
0009-8981(1997)268:1-2<85:MOS>2.0.ZU;2-Z
Abstract
This study reports on the ability of myocrisin to mediate in the produ ction and detoxification of oxidants (principally hydrogen peroxide) i n the monocyte in-vivo and in-vitro. The hydrogen peroxide produced by the monocyte derived from rheumatoid arthritis patients being treated with myocrisin was found to be 14.9+/-1.6 nmoles/10(6) cells and is e levated above levels found in monocytes obtained from patients either being treated with non-steroidal anti-inflammatory drugs (NSAIDs) (11. 3+/-0.4 nmoles/10(6) cells; P < 0.01) or normal healthy volunteers (11 .2+/-1.2 nmoles/10(6) cells; P < 0.01). A comparative study on glutath ione (GSH) oxidation indicated that levels of monocyte GSH were elevat ed in myocrisin-treated patients (2.40+/-0.49 mmol/l) over normal heal thy volunteers (0.83+/-0.18 mM; P < 0.01) and that levels of monocyte diglutathione (GSSG) were depressed (myocrisin, 0.97+/-0.41 mu mol/l; normal, 5.71+/-0.73 mu mol/l; P < 0.01). The non-inhibition of glutath ione reductase and the inhibition of glutathione peroxidase by gold pr ovides the link between these two observations. Thus, gold therapy wou ld seem to elevate monocyte hydrogen peroxide, increase monocyte reduc ed glutathione and decrease plasma glutathione peroxidase activity. Su bsequently, the data from this small group of patients (n = 10) provid es an indication that, in-vivo, myocrisin contributes to an increase i n oxidative stress. (C) 1997 Elsevier Science B.V.