Plasma total antioxidant capacity, lipid peroxidation, and erythrocyte antioxidant enzyme activities in patients with rheumatoid arthritis and osteoarthritis Sezgin Sarban a, * , Abdurrahim Kocyigit b , Mithat Yazar a , Ugur E. Isikan a a Department of Orthopaedic Surgery, Harran University, Medical Faculty, 63200 Sanliurfa, Turkey b Department of Biochemistry, Harran University, Medical Faculty, 63200 Sanliurfa, Turkey Received 22 June 2005; received in revised form 2 August 2005; accepted 15 August 2005 Available online 16 September 2005 Abstract Objectives: The metabolism of cells in inflammatory and noninflammatory arthritic joint diseases is subject to complex environmental controls. The aim of the present study was to investigate the total antioxidant capacity (TAC), levels of lipid peroxidation (LPO), and antioxidant enzyme activities in patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Design and methods: Plasma levels of TAC, malondialdehyde (MDA), the activities of some erythrocyte antioxidant enzymes, as well as erythrocyte sedimentation rates (ESR) were estimated in patients with RA and OA and compared with controls. Results: The plasma TAC levels were significantly lower in the RA group than the OA and control group (P < 0.05). Plasma MDA concentrations were significantly higher in patients with RA than those with OA and healthy subjects (P < 0.05). Erythrocyte GSH-Px and CAT activities were found to be significantly lower in patients with RA than those with OA and healthy subjects (P < 0.05, P < 0.05, respectively). However, there were no significant differences in erythrocyte SOD activities between the groups (P > 0.05). ESR were significantly higher in RA patients than in healthy subjects and patients with OA (P < 0.01). Moreover, there were significant negative correlations between TAC vs. MDA, ESR vs. TAC, and a positive correlation between ESR vs. MDA in the RA group (r = 0.398, P < 0.05; r = 0.422, P < 0.05; r = 0.530, P < 0.05, respectively). Conclusions: Our results demonstrated that levels of LPO are increased in patients with RA compared to patients with OA. In addition, plasma TAC levels are decreased in RA due to its inflammatory character. We conclude that detecting plasma TAC levels with this novel method may be used as a routine and rapid test to verify the levels of oxidative stress in RA. Furthermore, correlating TAC and LPO levels with acute phase reactants such as ESR may give some clues about disease activity in RA. D 2005 The Canadian Society of Clinical Chemists. All rights reserved. Keywords: Rheumatoid arthritis; Osteoarthritis; Antioxidant enzymes; Lipid peroxidation; Total antioxidant capacity Introduction Rheumatoid arthritis (RA) is a chronic progressive autoim- mune disorder characterized by symmetric erosive synovitis and sometimes shows multisystem involvement. The long-term outcome of this disease is characterized by significant morbidity, loss of functional capacity, and increased mortality. This disease affects about 1% of the general population worldwide [1,2]. Osteoarthritis (OA) generally consists of progressive loss of articular cartilage accompanied by attempted repair of articular cartilage, remodeling, and sclerosis of subchondral bone, with the formation of subchondral bone cysts and marginal osteo- phytes in many instances. Pathologically, the disease is characterized by fissuring and focal erosive cartilage lesions, as well as cartilage loss and destruction [3]. Although the pathophysiological basis of RA is not yet fully understood, reactive oxygen species (ROS) have been impli- 0009-9120/$ - see front matter D 2005 The Canadian Society of Clinical Chemists. All rights reserved. doi:10.1016/j.clinbiochem.2005.08.003 Abbreviations: RA, rheumatoid arthritis; OA, osteoarthritis; ROS, reactive oxygen species; BMI, body mass index; ESR, erythrocyte sedimentation rate; TAC, total antioxidant capacity; MDA, malondialdehyde; LPO, lipid peroxida- tion; GSH-Px, glutathione peroxidase; SOD, superoxide dismutase; CAT, catalase. * Corresponding author. Emniyet Caddesi Kultur Sokak Sembol Apt., No: 17/10, Yenisehir, 63100 Sanliurfa, Turkey. Fax: +90 414 315 11 81. E-mail address: sezginsarban@harran.edu.tr (S. Sarban). Clinical Biochemistry 38 (2005) 981 – 986