Endogenous mechanisms of reactive oxygen species (ROS) generation.

The main cellular source of reactive oxygen species (ROS) is mitochondrial respiratory chain and active NADPH responsible for "respiratory burst" of phagocytes. Whatsmore ROS are produced in endoplasmic reticulum, peroxisomes, with the participation of xanthine and endothelial oxidase and during autoxidation process of small molecules. Mitochondrial respiratory chain is the main cellular source of ROS.

Anti-MCV and anti-CCP antibodies-diagnostic and prognostic value in children with juvenile idiopathic arthritis (JIA).

The goal of the study was to evaluate the diagnostic and prognostic value of anti-mutated citrullinated vimentin (anti-MCV) antibodies in juvenile idiopathic arthritis (JIA) comparing to anti-cyclic citrullinated peptide (anti-CCP). Thirty children with confirmed JIA diagnosis and 20 children as a control group were included into the study. Serum and synovial fluid levels of anti-CCP, anti-MCV, and immunoglobulin M rheumatoid factor (IgM-RF) antibodies have been assessed.

[The role of reactive oxygen species (ROS) in arrhythmogenesis].

Reactive oxygen species (ROS) are the molecular oxygen derivatives that have at least one unpaired electron. Thus, ROS easily react with a number of cell structures causing a change in their functions. ROS produced in small quantities positively affect many cellular mechanisms, but in excess are responsible for the formation of oxidative stress.

Reactive oxygen species and serum antioxidant defense in juvenile idiopathic arthritis.

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.

Long-term melatonin administration enhances the antioxidant potential of human plasma maintained after discontinuation of the treatment.

We investigated the effect of long-term oral melatonin administration on the antioxidant capacity of plasma. The study was performed on healthy volunteers divided into two groups: the control group (without melatonin treatment) and the study group treated with 6 mg of melatonin per day for two weeks, 2 hours before bedtime. Blood samples were drawn: before melatonin administration, on the 7th and 14th day of melatonin treatment and on the 10th day after the last dose of melatonin.