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Animal models of rheumatoid arthritis (RA) are widely used for testing potential new therapies for RA. The most commonly used models of human RA are adjuvantinduced arthritis (AIA) and collagen-induced arthritis in rats and mice. In this chapter, we will focus on inflammatory and oxidative stress (OS) processes during the development of AIA. OS is a result of increased production of reactive oxygen species (ROS) or a reduction in the body’s endogenous antioxidant defense system. ROS and reactive nitrogen species (RNS) can contribute to the pathogenesis of RA by the induction of membrane oxidation, irreversible damage to proteins and DNA, cartilage damage, and induction of bone resorption. ROS/RNS can also modulate a variety of signaling events that control gene expression and affect cellular processes that participate in chronic inflammation. Our research team has been studying the course of OS during the development of rat AIA for more than a decade. We have analyzed the course of OS using markers of lipid peroxidation (malondialdehyde, 4hydroxy-2-nonenal, and F-2 isoprostanes), protein carbonyls, antioxidant enzymes (heme oxygenase and gamma-glutamyl transferase), and levels of endogenous antioxidants (coenzyme Q10 and Q9, gamma-tocopherol) in plasma and different tissues (joint, liver, lung, skeletal muscle, and spleen).

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Impact of Oxidative Stress on Inflammation in Rheumatoid and Adjuvant Arthritis: Damage to Lipids, Proteins, and Enzymatic Antioxidant Defense in Plasma and Different Tissues