The glutathione defense system in the pathogenesis of rheumatoid arthritis
β Scribed by M. Q. Hassan; R. A. Hadi; Z. S. Al-Rawi; V. A. Padron; S. J. Stohs
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 53 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0260-437X
- DOI
- 10.1002/jat.736
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β¦ Synopsis
Abstract
In order to assess a possible role of the natural glutathione defense system in the pathogenesis of rheumatoid arthritis (RA), serum reduced glutathione levels (GSH), glutathione reductase (GSR), glutathione Sβtransferase (GST), glutathione peroxidase (GSHβPx) and alkaline phosphatase (ALP) activities, lipid peroxidation (MDA content) and indexes of inflammation were evaluated in 58 rheumatic patients. Rheumatoid athritis was associated with significant depletion (ca. 50%) in GSH levels compared with normal control subjects. Serum levels of the detoxifying enzymes GSR and GSHβPx decreased by ca. 50% and 45%, respectively, whereas a threefold increase in the activity of GST was observed. A 1.2βfold increase in ALP was observed in patients with RA. These effects were accompanied by a 3.1βfold increase in serum MDA content. The MDA content was higher in RA patients who were seropositive for rheumatoid factor as well as positive for Cβreactive proteins. The erythrocyte sedimentation rate for all patients with RA was approximately 13.8βfold higher than for the control group, and was higher among RA patients who were positive for Cβreactive proteins and exhibited seropositivity for rheumatoid factor. Patients with RA receiving gold therapy exhibited significantly lower MDA levels whereas all other factors that were measured were not effected. The results support a hypothesis that defense mechanisms against reactive oxygen species are impaired in RA. Copyright Β© 2001 John Wiley & Sons, Ltd.
π SIMILAR VOLUMES
Accumulated knowledge of the inflammatory process in rheumatoid arthritis has been effectively summarized in recent years (1-4). Although the data are only circumstantial, the favored hypothesis is that an immune response to an as yet unknown antigen leads to the development of acute inflammation in
URING THE PAST FEW YEARS there has been a renewal of interest D in the study of synovial fluid. One recent development has been the demonstration of unusual inclusion bodies within the leukocytes present in inflammatory effusions. While not exclusively limited to rheumatoid arthritis, the phenomenon