Antioxidant gap and lipid peroxidation in patients with rheumatoid arthritis: Relationship to disease manifestations and activity

Citrullinated synovial antigens and the antibodies produced against them play a important role in the path physiology of RA[1]. Anti-CCP antibody positivity seems to be associated with increased synovial fluid oxidant activity (increased MDA and MPO levels) in patients with RA[2]. Excessive free radical production rather than impaired antioxidant enzymes activity due to autoantibody inhibition is been found in RA[3]. Antioxidant defenses protect the body from the detrimental effects of free radicals[4]. Blood contains many antioxidant molecules those prevent and/or inhibit harmful free radical reactions[5]. Albumin, the most abundant circulating protein in the plasma, exerts important antioxidant activities[6]. ROS, may cause a damage where they modify the antioxidant properties of albumin[7]. Uric acid formation may even provide a significant antioxidant defense mechanism against nitration by peroxynitrite during hypoxia[8]. The serum “antioxidant gap” reflects the antioxidant activity of ascorbate, alpha tocopherol, carotene, bilirubin and radical scavenging antioxidants other than albumin and uric acid[9]. There has been well documented the role of oxidative stress including redox state in autoimmune disease like RA[10-12]. However, relationship of antioxidant gap and total antioxidant capacity which present total antioxidant in the plasma has still to be illuminated. Further, There are no studies depicting the correlation of antioxidant gap and lipid peroxidation which is consider as a vital oxidant involved in the tissue damage in rheumatoid arthritis. Thus, the aim of this study was to explore relationships between total antioxidant gap and lipid peroxidation with respect to the disease severity of RA, which may have further implications in understanding rheumatoid pathology and therapeutic management of the disease.