ORIGINAL ARTICLE S. Taysi á F. Polat á M. Gul á R.A. Sari á E. Bakan Lipid peroxidation, some extracellular antioxidants, and antioxidant enzymes in serum of patients with rheumatoid arthritis Received: 27 September 2001 / Accepted: 30 October 2001 / Published online: 18 December 2001 Ó Springer-Verlag 2001 Abstract The aims of our study were to assess whether the increased oxidative stress in in¯amed joints is re¯ected by serum lipid peroxidation and also to check alterations in the levels of extracellular antioxidants and antioxidant enzyme activities in patients with rheuma- toid arthritis. Serum malondialdehyde and ceruloplas- min levels and the activity of CuZn superoxide dismutase were higher, while transferrin levels and the activities of glutathione peroxidase and catalase were lower in patients n=37) than in healthy controls n=30). Disease activity score correlated positively with serum malondialdehyde level and CuZn superoxide dismutase activity. Probably, superoxide radicals in serum could be dismutated to produce hydrogen per- oxide by increased CuZn superoxide dismutase activity, but hydrogen peroxide could not have been detoxi®ed due to decreased activities of serum glutathione peroxi- dase and catalase. Hydrogen peroxide possibly con- verted to hydroxyl radical by iron due to lower transferrin level might have led to increased serum lipid peroxidation in patients with rheumatoid arthritis. Keywords Rheumatoid arthritis á Serum á Malondialdehyde á Antioxidant enzymes á Disease activity score Introduction Rheumatoid arthritis RA) is a chronic progressive autoimmune disorder characterized by symmetric, ero- sive synovitis and sometimes shows multisystem involvement [1, 2]. It aects about 1% of the population worldwide and may lead to progressive joint destruction, deformity, disability, and premature death [1, 2, 3]. The synovial ¯uid of the in¯amed rheumatoid joint has been swarmed with in¯ammatory cells including activated neutrophils, which produce large amounts of superoxide radical O 2 .± ), hydrogen peroxide H 2 O 2 ), and highly reactive hydroxyl radical OH . ) [4, 5]. Neu- trophils from synovial ¯uids of patients with RA show enhanced O 2 .± production, possibly because of their exposure to cytokines present in the synovial ¯uids [6, 7]. Ischemia and reperfusion during movements also con- tribute to the production of reactive oxygen species in the in¯amed joint [8]. If not scavenged, these reactive species may lead to widespread lipid, protein, and DNA damage [9]. Babior suggests that reactive oxidants are important mediators in the pathogenesis of RA according to the studies related to oxidant damage and phagocyte function in these patients [10]. Cells have dierent antioxidant systems, including low molecular weight antioxidant molecules like gluta- thione [11] and various antioxidant enzymes, to defend themselves against free radical attacks [12]. Superoxide dismutase SOD), the ®rst line of defense against oxygen- derived free radicals, catalyzes the dismutation of the superoxide anion O 2 .± ) into hydrogen peroxide H 2 O 2 ). H 2 O 2 can be transformed into H 2 O and O 2 by catalase. Glutathione peroxidase GSH-Px) is a selenoprotein Rheumatol Int 2002) 21: 200±204 DOI 10.1007/s00296-001-0163-x S. Taysi &) á E. Bakan Department of Biochemistry, Faculty of Medicine, Ataturk University, 25240 Erzurum, Turkey E-mail: seytaysi@hotmail.com Tel.: +90-442-2312220 Fax: +90-442-2348470 F. Polat Biotechnology Application and Research Center, Ataturk University, Erzurum, Turkey M. Gul Department of Physiology, Faculty of Medicine, Ataturk University, Erzurum, Turkey R.A. Sari Department of Immunology, Faculty of Medicine, Ataturk University, Erzurum, Turkey