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

内分泌学 脾脏 超氧化物歧化酶 谷胱甘肽过氧化物酶 内科学 关节炎 丙二醛 谷胱甘肽还原酶 氧化应激 谷胱甘肽 医学 化学 抗氧化剂 生物化学
作者
Eun‐Mi Choi
出处
期刊:Journal of Applied Toxicology [Wiley]
卷期号:27 (5): 472-481 被引量:27
标识
DOI:10.1002/jat.1228
摘要

Abstract 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 β , 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 © 2007 John Wiley & Sons, Ltd.

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