OBJECTIVES: To investigate the relationship between carbonic anhydrase (CA) II autoantibody and lipid peroxidation, certain antioxidant parameters, and cytokines in rheumatoid arthritis (RA) patients. DESIGN AND METHODS: Serum levels of CA II autoantibody, cytokines (TNFα, IL-6, IFN-γ, IL-1β) and bone markers (crosslaps, osteocalcine) and erythrocyte levels of antioxidant enzyme activities (SOD, CAT, GPx), GSH and MDA, and CA activities were measured in RA patients and healthy controls. RESULTS: The CA II autoantibody titers were significantly higher (P<0.05), and erythrocyte SOD activities were significantly lower (P<0.05) in RA patients. A significant negative correlation between CA II autoantibody titers and SOD activities in RA group was established (r=-0.430, p=0.006). The elevated cytokine levels could not be correlated with CA II autoantibody levels in RA. CONCLUSION: These results suggest that increased erythrocyte oxidative stress observed in RA may be effective in the mechanism of CA II autoantibody formation.
OBJECTIVES: To investigate the relationship between carbonic anhydrase (CA) II autoantibody and lipid peroxidation, certain antioxidant parameters, and cytokines in rheumatoid arthritis (RA) patients. DESIGN AND METHODS: Serum levels of CA II autoantibody, cytokines (TNFα, IL-6, IFN-γ, IL-1β) and bone markers (crosslaps, osteocalcine) and erythrocyte levels of antioxidant enzyme activities (SOD, CAT, GPx), GSH and MDA, and CA activities were measured in RApatients and healthy controls. RESULTS: The CA II autoantibody titers were significantly higher (P<0.05), and erythrocyte SOD activities were significantly lower (P<0.05) in RApatients. A significant negative correlation between CA II autoantibody titers and SOD activities in RA group was established (r=-0.430, p=0.006). The elevated cytokine levels could not be correlated with CA II autoantibody levels in RA. CONCLUSION: These results suggest that increased erythrocyte oxidative stress observed in RA may be effective in the mechanism of CA II autoantibody formation.
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