4.5 Article

Oxidative status of DBA/1J mice with type II collagen-induced arthritis

Journal

JOURNAL OF APPLIED TOXICOLOGY
Volume 27, Issue 5, Pages 472-481

Publisher

WILEY
DOI: 10.1002/jat.1228

Keywords

oxidant status; collagen-induced arthritis; DBA/1J mouse

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Funding

  1. National Research Foundation of Korea [2004-206-E00013] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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The present study was undertaken to compare the oxidant statuses of mice with collagen-induced arthritis (CIA) and those of healthy mice. For this purpose, serum oxidant products and arthritic profiles were measured in DBA/ 1J mice with CIA. In addition, the levels of oxidation products and the activities of antioxidant enzymes were determined in liver, heart, spleen, kidney, lung and brain. The induction of arthritis significantly increased anti-collagen antibody, rheumatoid factor, interleukin (IL)-1 beta, IL-6, protein carbonyl (PCO), advanced glycation end-products (AGE), malondialdehyde (MDA) and low density lipoprotein (LDL)-cholesterol levels in serum (P < 0.05). CIA in DBA/1J mice was associated with significantly lower activities of superoxide dismutase, glutathione peroxidase and glutathione reductase in spleen but higher levels of oxidation products in spleen, kidney and liver than healthy normal mice (P < 0.05). However, lower concentrations of oxidized protein and higher activities of antioxidant enzymes were observed in CIA mouse lung and brain than in healthy normal mice. Dexamethasone treated CIA mice had decreased arthritis-related indices and showed: reduced PCO and AGE in spleen and brain, and increased PCO and AGE in heart, kidney and lung; increased MDA in heart, spleen, lung and brain; reduced SOD and GR activities in lung and brain; increased GPx activity in spleen and brain; and increased GR activity heart and spleen. These data suggest that mice with CIA were more susceptible to oxidative damage in the spleen and liver under the chronic inflammatory conditions. Copyright (C) 2007 John Wiley & Sons, Ltd.

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