Background Known role of SC in the pathogenesis of RA. It is impossible, however, at this level of knowledge to ascertain all the mechanisms for their involvement in the pathological process. Reduced tissue antioxidant protection can affect cellular metabolism, and as might be expected, through the mechanism of autophagy inducing mitochondrial and lysosomal degradation, facilitating cell membrane depolarization.

Objectives The aim of this work was to study the electrophoretic mobility (EM) of SC of RA patients and its relationship with the activity of antioxidant enzymes: Cu-Zn superoxidismutase (Cu-Zn SOD), Se-glutathione peroxidase (Se-GPO) and catalase (the CAT) in synovial fluid (SF).

Methods SF has been obtained from the knee of 7 patients with RA and 5 donors. SC isolated by standard methods. EM of SC determined by the automatic microscope. Se level in SF recorded by atomic absorption spectrometry. The activity of the antioxidant enzymes was determined by classical methods of enzymology.

Results A significant depolarization of the RA SC, resulting in a reduction of their EM as compared to the normal level of the average in 4 times. Activity of antioxidant enzymes is dramatically reduced by a significant decrease of Se concentrations in SF (150 μg/l normally up to 80 μ g/l in RA), which is particularly reflected in the activity of Se GPO (note that SF can be up to 100 Se-containing proteins).

Conclusions We can assume that aggravated by RA catabolic processes that caused the dysfunction of the lysosomal and mitochondrial structures (autophagy), consistently shoot antioxidant protection of SC and cause depolarization and the decrease in electrophoretic mobility of these cells.

Disclosure of Interest None declared