Study on the relationship between protein oxidation and disease activity in systemic lupus erythematosus.
- Author:
Qun ZHANG
1
;
Dong-Qing YE
;
Guo-Ping CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Antibodies, Antinuclear; metabolism; DNA; metabolism; Enzyme-Linked Immunosorbent Assay; Female; Humans; Lupus Erythematosus, Systemic; blood; metabolism; Male; Middle Aged; Oxidation-Reduction; Peroxidase; metabolism; Proteins; metabolism; Superoxide Dismutase; metabolism; Young Adult
- From: Chinese Journal of Epidemiology 2008;29(2):181-184
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo examine the levels of protein oxidation in systemic lupus erythematosus (SLE) and to evaluate the relation between oxidative protein damage and disease activity index.
METHODSPlasma was collected from SLE patients and healthy subjects as controls. Protein-bound carbonyls, protein thiols, superoxide dismutase (SOD), myeloperoxidase (MPO) and total antioxidant capacity (TAOC) were determined by spectrophotometry. Levels of anti-double-stranded DNA (anti-dsDNA) and antinuclear antibody (ANA) were quantified by enzyme-linked immunosorbent assay.
RESULTSWhen comparing with the control subjects, SLE patients exhibited elevated levels of protein carbonyls [(0.101 +/- 0.033) nmol/mg, (0.061 +/- 0.019)nmol/mg, P < 0.01], degraded levels of protein thiols [(3.911 +/- 0.968) nmol/mg, (4.655 +/- 0.798) nmol/mg, P < 0.01] and activities of T-SOD [(67.01 +/- 12.22) U/ml, (97.35 +/- 14.11) U/ml, P < 0.01]. Levels of plasma protein thiols and activities of T-SOD were lower in SLE patients positive for anti-dsDNA antibody, compared with patients negative for anti-dsDNA antibody.
CONCLUSIONWe found that the elevated levels of multiple markers of protein oxidation and degraded activities of antioxidant enzymes in plasma from SLE patients existed when comparing with the controls, and the all the levels were correlated with disease activity. Our findings suggested that protein oxidation might play a role in the pathogenesis of chronic organ damage in SLE.