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Oxidative protein damage and antioxidant status in systemic lupus erythematosus
Author(s) -
Zhang Q.,
Ye D. Q.,
Chen G. P.,
Zheng Y.
Publication year - 2010
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/j.1365-2230.2009.03437.x
Subject(s) - oxidative stress , superoxide dismutase , catalase , erythrocyte sedimentation rate , antioxidant , pathogenesis , glutathione peroxidase , glutathione , medicine , immunology , lupus erythematosus , myeloperoxidase , endocrinology , chemistry , biochemistry , enzyme , antibody , inflammation
Summary Background. Oxidative stress may play a role in the pathogenesis of systemic lupus erythematosus (SLE). Proteins are one of the main targets for oxidants, due to their abundance in biological systems and their high rate constants for reaction. Aim. To evaluate differences in oxidative protein damage and antioxidant status between patients with SLE and healthy controls, and to explore whether oxidative protein damage has a role in either the disease activity or the organ damage in SLE. Methods. Using spectrophotometry and ELISA, the levels of multiple markers of protein oxidation and antioxidant status in the serum of 62 patients with SLE and 62 healthy controls were evaluated. Results. We found that levels of multiple markers of protein oxidation and activities of superoxide dismutase (SOD) and myeloperoxidase were increased, whereas levels of protein thiol and activities of glutathione peroxidase and catalase were reduced in serum from patients with SLE compared with controls. Disease activity index correlated positively with erythrocyte sedimentation rate and levels of serum protein carbonyl (PC), 3‐nitrotyrosine and C‐reactive protein, and negatively with levels of serum protein thiols and activities of SOD, glutathione peroxidase and catalase activities in patients. There was a significant difference in the serum PC levels between patients with and without arthritis or arthralgia. The same was true when patients with and without cardiac involvement, and patients with and without renal disease were analysed. Conclusions. The findings suggest that protein oxidation may play a role in the pathogenesis of chronic organ damage in SLE.