Abstract
Rheumatoid arthritis (RA) as a chronic inflammatory disease is associated with oxidative stress. Drugs targeting tumor necrosis factor-alpha (TNF-α) ameliorate inflammation and symptoms of RA in most patients. Whether markers of oxidative stress can be used for monitoring of treatment effects is unknown. The aim of our study was to analyze the effects of anti-TNF-α treatment on oxidative stress in plasma and saliva of patients with RA. Samples were collected from 26 patients with RA at baseline as well as 3 and 6 months after starting the anti-TNF-α treatment. Thiobarbituric acid-reacting substances (TBARS), advanced oxidation protein products (AOPP), advanced glycation end products (AGEs), and fructosamine were quantified using spectrophotometry and spectrofluorometry in plasma. TBARS were measured also in saliva. The disease activity score (DAS28) was used to assess the clinical status of patients. No significant dynamic changes were found except plasma TBARS that decreased continuously. At 6 months after starting the treatment, plasma TBARS were lower by 39% in comparison to baseline (p = 0.006). Salivary concentrations of TBARS did not reflect the dynamics in plasma. Although a trend was observed (r = 0.33), a significant correlation between plasma TBARS and DAS28 was not found. Our results indicate that anti-TNF-α treatment decreases plasma TBARS as a marker of lipid peroxidation. However, the lack of a significant correlation with DAS28 suggests that it cannot be used for monitoring of treatment. Other markers of oxidative stress and antioxidant capacity with lower biological variability should be tested in future studies.
Highlights
Rheumatoid arthritis (RA) is a chronic inflammatory disease [1]
The results showed that the median concentration of Thiobarbituric acid-reacting substances (TBARS) in plasma of patients with RA decreased by 12% 3 months
The results of our study show that the lipid peroxidation marker TBARS is decreased by the anti-inflammatory
Summary
The inflammation is not restricted to the joints; it is rather systemic [2]. The modifications are often mediated by oxidative or carbonyl stress [5]. Oxidative stress is a dysbalance between the production of reactive oxidants and antioxidant mechanisms [6]. The overproduction of free radicals or a lower production of antioxidants leads to oxidation of various macromolecules, especially lipids and proteins. Chronic inflammation is a common cause of oxidative stress [7, 8]. Mainly neutrophils and macrophages, enzymatically produce reactive oxygen species to fight against bacteria and other microorganisms [9]. In case of chronic sterile inflammation, the prolonged overproduction of reactive oxygen species leads to oxidative damage of tissues [10]
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