The glutathione defense system in the pathogenesis of rheumatoid arthritis (類風濕性關節炎) PY2001 IR95
在 類風濕性關節炎 發病過程中的 穀胱甘肽 防禦系統
資訊來源 2023-0612：
https://pubmed.ncbi.nlm.nih.gov/11180282/
#湯偉晉挑選的醫學論文
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J Appl Toxicol
2001 Jan-Feb;21(1):69-73. doi: 10.1002/jat.736.
The glutathione defense system in the pathogenesis of rheumatoid arthritis
在 類風濕性關節炎 發病過程中的 穀胱甘肽 防禦系統
M Q Hassan 1 , R A Hadi, Z S Al-Rawi, V A Padron, S J Stohs
Affiliation
1 Faculty of Pharmacy & Medical Sciences, Amman University, Amman 19328, Jordan.
PMID: 11180282 DOI: 10.1002/jat.736
Abstract
In order to assess a possible role of the natural glutathione defense system in the pathogenesis of rheumatoid arthritis (類風濕性關節炎) (RA), serum reduced glutathione levels (GSH), glutathione reductase (GSR), glutathione S-transferase (GST), glutathione peroxidase (GSH-Px) and alkaline phosphatase (ALP) activities, lipid peroxidation (MDA content) and indexes of inflammation were evaluated in 58 rheumatic patients.
重點
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 GSH-Px decreased by ca. 50% and 45%, respectively, whereas a threefold increase in the activity of GST was observed.
A 1.2-fold increase in ALP was observed in patients with RA. These effects were accompanied by a 3.1-fold increase in serum MDA content. The MDA content was higher in RA patients who were seropositive for rheumatoid factor as well as positive for C-reactive proteins.
重點
The erythrocyte sedimentation rate for all patients with RA was approximately 13.8-fold higher than for the control group, and was higher among RA patients who were positive for C-reactive 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.
重點
The results support a hypothesis that defense mechanisms against reactive oxygen species are impaired in RA.
Copyright 2001 John Wiley & Sons, Ltd.
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