Erythrocyte reduced/oxidized glutathione and serum thiol/disulfide homeostasis in patients with rheumatoid arthritis.
Disulfide
Glutathione
Oxidative stress
Rheumatoid arthritis
Thiol
Journal
Clinical biochemistry
ISSN: 1873-2933
Titre abrégé: Clin Biochem
Pays: United States
ID NLM: 0133660
Informations de publication
Date de publication:
Aug 2021
Aug 2021
Historique:
received:
09
12
2020
revised:
13
03
2021
accepted:
25
04
2021
pubmed:
3
5
2021
medline:
10
8
2021
entrez:
2
5
2021
Statut:
ppublish
Résumé
Chronic inflammation and oxidative stress are the most known mechanisms in Rheumatoid Arthritis (RA) pathophysiology, which is still not fully elucidated. In this study, we evaluated oxidative status by determining intracellular reduced/oxidized glutathione (GSH/GSSG) homeostasis and serum thiol/disulfide (SH/SS) homeostasis in RA patients. A total of 152 RA patient and 89 healthy controls were included in the study. RA patients were subdivided according to disease activity score-28 (DAS-28) as active RA and remission RA. Intracellular GSH/GSSG and serum SH/SS homeostasis parameters were analyzed. Median (1st-3rd quartile values) SS/SH and GSSG/GSH percent ratio levels were significantly higher in RA patients (6.94 (6.02-8.54) and 69.8 (44.05-85.29); respectively) compared to controls (4.62 (4.15-5.46) and 34.9 (22.43-62.2); respectively) (p < 0.05 for all). SS/SH and GSSG/GSH percent ratio levels were significantly higher in active RA patients when compared to remission RA patients and controls (p < 0.05 for all). SS/SH and GSSG/GSH percent ratios were significantly increased in remission RA group compared to controls (p < 0.05 for all). DAS28 scores were positively correlated with SS/SH and GSSG/GSH percent ratios (rho = 0.259 and 0.296; respectively). These findings suggest that active intracellular and extracellular thiol group oxidation process might play a role in RA pathogenesis and further work in these areas may be warranted to show potential value of evaluating intracellular GSSG/GSH and serum SH/SS balances together in disease monitoring.
Sections du résumé
BACKGROUND
BACKGROUND
Chronic inflammation and oxidative stress are the most known mechanisms in Rheumatoid Arthritis (RA) pathophysiology, which is still not fully elucidated. In this study, we evaluated oxidative status by determining intracellular reduced/oxidized glutathione (GSH/GSSG) homeostasis and serum thiol/disulfide (SH/SS) homeostasis in RA patients.
METHODS
METHODS
A total of 152 RA patient and 89 healthy controls were included in the study. RA patients were subdivided according to disease activity score-28 (DAS-28) as active RA and remission RA. Intracellular GSH/GSSG and serum SH/SS homeostasis parameters were analyzed.
RESULTS
RESULTS
Median (1st-3rd quartile values) SS/SH and GSSG/GSH percent ratio levels were significantly higher in RA patients (6.94 (6.02-8.54) and 69.8 (44.05-85.29); respectively) compared to controls (4.62 (4.15-5.46) and 34.9 (22.43-62.2); respectively) (p < 0.05 for all). SS/SH and GSSG/GSH percent ratio levels were significantly higher in active RA patients when compared to remission RA patients and controls (p < 0.05 for all). SS/SH and GSSG/GSH percent ratios were significantly increased in remission RA group compared to controls (p < 0.05 for all). DAS28 scores were positively correlated with SS/SH and GSSG/GSH percent ratios (rho = 0.259 and 0.296; respectively).
CONCLUSIONS
CONCLUSIONS
These findings suggest that active intracellular and extracellular thiol group oxidation process might play a role in RA pathogenesis and further work in these areas may be warranted to show potential value of evaluating intracellular GSSG/GSH and serum SH/SS balances together in disease monitoring.
Identifiants
pubmed: 33933432
pii: S0009-9120(21)00141-7
doi: 10.1016/j.clinbiochem.2021.04.023
pii:
doi:
Substances chimiques
Disulfides
0
Sulfhydryl Compounds
0
Glutathione Disulfide
ULW86O013H
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
56-61Informations de copyright
Copyright © 2021 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.