Background Intra-articular dynamics of free radical processes in RA and OA reflects the degree of cellular destruction and the depth of the membrane pathological changes. Multi-component antioxidant system hinders the development of these negative phenomena.
Objectives We studied the dynamics of free radical processes (the rate of lipid peroxidation (LPO - the level of malondialdehyde - MDA), activity of phospholipase (PHL-A2) and phospholipids - PHL) and the antioxidant defense system (activity superoxiddismutase (SOD), catalase (CAT), glutathione-S-transferase (G-S-T), tocopherols (TF) and ceruloplasmin (CP) in SF of patients with RA and OA. The data were compared with the levels of inflammation cytokines.
Methods Investigated the SG of the knee in 15 patients with RA and 15 patients with OA, female, age 50±12 years. Besides the well-known methods of biochemistry and enzymology, for determining the activity of PHL-A2 used immunoassay method and reagent kits of company “Cayman chemical”, analysis of cytokines was performed enzymelinked immunosorbent method.
Results In OA, and especially in RA in SF, with the intensification of free radical processes (intensified the breakdown of phospholipids, increases the level MDA – secondary product of LPO and marker of degradation of membrane structures). Against this background, the observed inhibition of the antioxidant defense system (decreased activity of SOD, CAT, G-ST – enzyme conjugates with glutathione toxic products LPO and promotes their excretion; reduced level TF, designed to stabilize the lipid composition of membranes and protect them from degradation caused PHL-A2, and also block the damaging effect of singlet oxygen; also dramatically reduced the level of CP, which neutralizes free radicals). These changes are consistent with activation in SF with RA and OA proinflammatory cytokines and TNF-α. Table 1.Free radicals, antioxidant defense system and cytokine status of SF with RA and OA
Conclusions Intensification of free radical processes, generation of reactive oxygen species as a result of suppression of antioxidant protection is a cause of metabolic disorders of proteins and lipids in LF with RA and OA, the cause of the inflammatory process that causes apoptosis and cell destruction. The current strategy for the treatment of RA and OA is focused on reducing pain and preventing progressive degeneration of articular cartilage and subchondral bone, based on identified pathogenetic mechanisms, such as the development of inflammation and tissue destruction caused by the activation of free radical processes, suppression of antioxidant protection, dynamics of proinflammatory cytokines and TNF-α.
Disclosure of Interest None declared