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Updated: May 2, 2026

Evaluation of Oxidative Stress in Biological Samples Using the Thiobarbituric Acid Reactive Substances Assay
Published on: May 12, 2020
Reactive oxygen species and serum antioxidant defense in juvenile idiopathic arthritis
Joanna Lipińska1, Stanisława Lipińska, Jerzy Stańczyk
1Department of Pediatric Cardiology and Rheumatology, Second Chair of Pediatrics, Medical University of Lodz, 36/50 Sporna St, 91-738, Lodz, Poland, joanna-lipinska@wp.pl.
Abstract:
In autoimmune inflammatory diseases, including juvenile idiopathic arthritis (JIA), which leads to joint destruction, there is an imbalance between production of reactive oxygen species (ROS) and their neutralization which, as a consequence, leads to "oxidative stress." The aim of the study was to assess the concentration of oxidative stress markers: nitric oxide (NO), a degree of lipid membrane damage, and total antioxidant plasma capacity in children with JIA. Thirty-four children with JIA were included into the study. A degree of lipid membrane damage (lipid peroxidation products) was estimated as thiobarbituric acid-reactive substances (TBARs), NO concentration as NO end-products: nitrite/nitrate (NO2(-)/NO3(-)) and total antioxidant plasma capacity as ferric reducing ability of plasma (FRAP). NO2(-)/NO3(-) serum concentration in children with JIA was statistically significantly higher than that in healthy children (p = 0.00069). There was no significant difference in TBAR levels between children with JIA and the control group. FRAP in sera of children with JIA was lower than that in healthy children, but the difference was not statistically significant. A statistically significant positive correlation was observed between NO end products and the 27-joint juvenile arthritis disease activity score (JADAS-27) and ESR, and a negative correlation was observed between FRAP and C-reactive protein (CRP) and white blood cell count (WBC). Our results confirm the increased oxidative stress in children with JIA. Overproduction of NO and decrease in the antioxidant plasma capacity may be involved in JIA pathogenesis.
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