Abstract
Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease with a global prevalence of 0.5–1.0% of the adult population and projected 80% increase in incidence by 2050 [6]. Oxidative stress plays a fundamental role in RA pathogenesis through reactive oxygen species generated by activated synoviocytes and infiltrating leukocytes, leading to cartilage degradation, chondrocyte apoptosis and pannus formation [4]. Malondialdehyde (MDA) is the most accessible biomarker of oxidative stress and reflects ongoing lipid peroxidation [4]. Mitochondrial superoxide dismutase 2 (SOD2, MnSOD) is a key enzyme of mitochondrial antioxidant defense; the functional polymorphism Ala16Val (rs4880) reduces enzyme transport into mitochondria with subsequent activity reduction by 30–40% [3, 7]. Significant associations of SOD2 Ala16Val with RA activity have been established in European populations [2], but data on Central Asian ethnic groups remain limited.
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