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Published on: May 22, 2015
Abnormal sulphur oxidation in systemic lupus erythematosus
C Gordon1, H Bradley, R H Waring
1Department of Rheumatology, University of Birmingham, UK.
Lancet (London, England)
|January 4, 1992
Summary
Systemic lupus erythematosus (SLE) patients exhibit impaired S-oxidation, a key sulfur metabolism pathway. This study highlights a distinct biochemical difference in sulfur metabolism between SLE and rheumatoid arthritis.
Area of Science:
- Biochemistry
- Immunology
- Metabolic pathways
Background:
- Sulfur metabolism plays a crucial role in biological systems.
- Alterations in metabolic pathways are implicated in autoimmune diseases like SLE.
- Understanding sulfur metabolism in SLE can reveal disease-specific biomarkers.
Purpose of the Study:
- To investigate the activity of the S-oxidation pathway of sulfur metabolism in patients with systemic lupus erythematosus (SLE).
- To compare sulfur metabolism in SLE patients with healthy controls.
- To differentiate sulfur metabolism profiles between SLE and rheumatoid arthritis (RA).
Main Methods:
- Utilized S-carboxy-L-methylcysteine as a probe to assess S-oxidation activity.
- Measured substrate/product ratios for cysteine oxygenase (plasma cysteine/sulfate).
- Evaluated the S-methylation pathway catalyzed by thiolmethyltransferase.
Main Results:
- A significant majority of SLE patients (71%) displayed impaired sulphoxidation.
- 25% of SLE patients showed virtually no sulphoxide production, compared to 4% in controls.
- The cysteine oxygenase pathway was significantly upregulated in SLE patients (p < 0.00001).
- The S-methylation pathway remained unimpaired in SLE patients.
Conclusions:
- SLE is characterized by impaired S-oxidation, a key pathway in sulfur metabolism.
- The S-methylation pathway is not affected in SLE patients.
- Sulfur metabolism exhibits distinct differences between SLE and RA, with both pathways impaired in RA.
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