The aim of this study was to assess the oxidative stress status in rheumatoid arthritis (RA) by measuring markers of free radical production, systemic activity of disease, and levels of antioxidant. 52 RA patients and 30 healthy controls were included in the study, and clinical examination and investigations were performed and disease activity was assessed. Peripheral blood samples were used for all the assays. We assessed the markers of oxidative stress, including plasma levels of index of lipid peroxidation-thiobarbituric acid reactive substances (TBARS), hydrogen peroxide (H₂O₂), superoxide anion radical (O₂(-)), nitric oxide (NO), and superoxide dismutase activity (SOD), catalase activity (CAT) and glutathione levels in erythrocytes. In the RA group, levels of H₂O₂, O₂(-), and TBARS were significantly higher than in controls (4.08 ± 0.31 vs. 2.39 ± 0.13 nmol/l, p < 0.01; 8.90 ± 1.28 vs. 3.04 ± 0.38 nmol/l, p < 0.01, 3.65 ± 0.55 vs. 1.06 ± 0.17 μmol/l, p < 0.01). RA patients had significantly increased SOD activity compared with healthy controls (2,918.24 ± 477.14 vs. 643.46 ± 200.63UgHbx103, p < 0.001). Patients had significantly higher levels of pro-oxidants (O₂(-), H₂O₂, and TBARS) compared to controls, despite significantly higher levels of SOD. Significant differences were also observed in serum levels of NO in patients with high-diseases activity. Our findings support an association between oxidative/nitrosative stress and RA. Stronger response in samples with higher diseases activity suggests that oxidative/nitrosative stress markers may be useful in evaluating the progression of RA as well as in elucidating the mechanisms of disease pathogenesis.

Although exercise-induced oxidative stress receives considerable scientific attention, there is still little information available regarding exercise-induced adaptations of the antioxidant defence system in adolescent and child athletes. The aim of our study was to establish the effects of long-term exercise training on the redox state of adolescents, and to find correlations between elements of redox homeostasis and aerobic power. Thirty-three handball players and 14 non-athletes, 16-19-years old, were subjected to blood sampling to measure levels of nitric oxide (NO; estimated through nitrites (NO₂⁻), superoxide anion radical (O₂⁻), hydrogen peroxide (H₂O₂), lipid peroxidation (estimated through TBARS), superoxide dismutase (SOD) and catalase (CAT). Subjects were also subjected to maximal progressive exercise test to estimate their maximal oxygen consumption (VO₂max). Athletes had significantly (P < 0.05) higher SOD activity and lower CAT activity compared with non-athletes (SOD: 2175.52 ± 362.07 compared with 1172.16 ± 747.40 U/g of hemoglobin x 10³, and CAT: 2.19 ± 0.31 compared with 3.08 ± 0.47 U/g of hemoglobin x 10³). These differences were the most obvious when comparing non-athletes and athletes with poor/average aerobic power. H₂O₂ and TBARS levels differed among subjects with poor, average or good aerobic power (P < 0.01, and P < 0.05, respectively). Sports engagement and aerobic capacity are important factors in inducing changes in redox status.

Abstract. The aims of our study were to assess the redox state of adolescent athletes and non-athletes both at rest and after acute exposure to physical load and to find relations between parameters of redox state and morphofunctional characteristics of subjects. 58 young handball players and 37 non-athletes were subjected to body composition analysis, measuring of maximal oxygen consumption and blood sampling immediately before and after a maximal progressive exercise test. At rest, athletes had significantly higher superoxide dismutase (SOD) and catalase (CAT) activity, higher levels of reduced glutathione (GSH) and nitric oxide (NO) and lower levels of lipid peroxidation (TBARS) compared with non-athletes. A maximal exercise test induced statistically significant rise of superoxide anion radical (O 2 -), hydrogen peroxide (H 2 O 2 ) and NO levels in non-athletes, while TBARS levels decreased. Athletes experienced the fall in NO levels and the fall in CAT activity. After exercise, athletes had significantly lower levels of O 2 -compared with non-athletes. Two way repeated measures ANOVA showed that the response of O 2 -, NO and TBARS to the exercise test was dependent on the sports engagement (training experience) of subjects. Significant correlations between morphofunctional and redox parameters were found. These results suggest that physical fitness affects redox homeostasis.

The purpose of this study was to assess the influence of sport-specific and nonspecific bouts of exercise on athletes' redox state. Blood samples were collected from 14 handball players immediately before and after graded exercise test on the cycle ergometer and handball training. Levels of superoxide anion radical (O2−), hydrogen peroxide (H2O2), nitrites (NO2−) as markers of nitric oxide, index of lipid peroxidation (TBARs), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activity were determined. Exercise intensity was assessed by a system for heart rate (HR) monitoring. Average athletes' HR was not significantly different between protocols, but protocols differed in total time and time and percentage of time that athletes spent in every HR zone. The laboratory exercise test induced a significant increase of H2O2 and TBARs as well as the decrease of the SOD and CAT activity, while after specific handball training, levels of NO2− were increased and SOD activity decreased. It seems that unaccustomed short intensive physical activity may induce oxidative stress in trained athletes, while sport-specific activity of longer duration and proper warm-up period may not. Further research should show whether the change of protocol testing and the implementation of various supplementations and manual methods can affect the redox equilibrium.

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