The levels of malondialdehyde, nitric oxide, the activity of xanthine oxidase and superoxide dismutase enzymes of patients with rheumatoid arthritis and systemic sclerosis

In healthy humans beings, the endogenous free radicals produced in the body are neutralized by endogenous antioxidants. But, the insufficiency of antioxidant defense systems or the acceleration of the oxidative reactions can result in the oxidative stress. Oxidative damage to essential cell components caused by oxygen free radicals has been proposed as an important mechanism in the pathogenesis of systemic sclerosis (SSc) and rheumatoid arthritis (RA). Systemic sclerosis is a chronic inflammatory disease characterized by vascular injury, immunological abnormalities and widespread fibrosis of skin and internal organs. Although the etiology of disease is unknown, It is thought that oxidative stress has an important role in the pathogenesis. Rheumatoid arthritis (RA) is a chronic disease characterized by inflammation in periferic joints. Although the pathophysiological basis of RA is not yet fully understood, some investigations have been shown that oxidative stress have implicated in its pathogenesis. In this study, the levels of malondialdehyde (MDA), nitric oxide (NO), the activity of xanthine oxidase (XO) and erythrocyte superoxide dismutase (SOD) enzymes of patients with rheumatoid arthritis and systemic sclerosis (SSc) were investigated. Forthy-two patients with systemic sclerosis (SSc), Forthy-three patients with rheumatoid arthritis and 40 healthy controls were taken into the study. The levels of serum MDA and serum NO, the activity of serum XO and erythrocyte SOD enzymes were determined. While patients with systemic sclerosis had significantly higher serum malondialdehyde (MDA) levels compared to normal subjects (p<0,008); there were no differance between rheumatoid arthritis groups and normal subjects (p= 1.00). Besides patients and the control group did not show any difference the level of serum NO, the activity of serum XO and erythrocyte SOD (p= 0.211, p= 0.593, p= 0.508). In conclusion, increased MDA levels in our study may be importance as a marker but are not sufficient to show that there is an increased oxidative stress in systemic sclerosis patients because supporting results were not obtained from SOD, NO and XO measurements. In addition, in our study the similarity in the levels of MDA, SOD, NO and XO in RA patients might be related to the remission phase of the disease.