The results of this study provide further evidence of the relationship between lipid peroxidation and cancer and should contribute to the interpretation of epidemiological studies in this area and the planning of future research.
The insufficiency of antioxidant defense systems and the acceleration of the oxidative reactions can be results of the pro-oxidant/antioxidant imbalance in rheumatoid arthritis (RA). The aim of our study was to investigate the changes in oxidant status by measuring two different parameters; one was the level of malondialdehyde (MDA) as an index of lipid peroxidation and the other was total oxidative status; we could then compare our results with the antioxidant status, superoxide dismutase (SOD) enyzme activities. All were assessed in 22 patients with active RA and 18 age- and gender-matched control subjects. While serum MDA levels were significantly increased in patients with RA compared to the control group (p<0.03), the total oxidative status levels were decreased in patients with RA compared to the control group (p<0.008), and serum SOD activities did not show any statistical difference between the two groups. In conclusion, the increased MDA levels in our study may be important as a marker but are not sufficient to conclude that there was an increase in oxidative stress in RA patients because supporting results were not obtained from SOD and oxidative status measurements. These results give further support to the concept of oxygen free radicals playing a role in the pathogenesis of chronic inflammatory disorders, but we also consider that there is a more complex relationship than has been assumed. We think that further studies are needed to clarify these conflicting results.
Free radicals are implicated in many diseases including atherosclerosis, cancer and also in rheumatoid arthritis. Reaction of uric acid with free radicals, such as hydroxyl radical and hypochlorous acid (HOCl) results in allantoin production. In this study, we measured the serum allantoin levels, oxidation products of uric acid, as a marker of free radical generation in rheumatoid arthritis. Fasting blood samples were obtained from 21 rheumatoid patients and 15 healthy controls. In this study, the serum allantoin and uric acid levels were measured by a gas chromatography-mass spectrometry method and the ratios were calculated. The mean allantoin and uric acid levels and ratios in the patient group were 22.1 +/- 11.3, 280.5 +/- 65.0 and 8.0 +/- 3.7 microM, while in the control group they were 13.6 +/- 6.3, 278.3 +/- 53.6 and 4.9 +/- 2.1 microM, respectively. The effects of gender, age, menopausal status, duration of disease and medications on serum allantoin and uric acid levels of the patient and control groups were studied. Our results suggest that uric acid acts as a free radical scavenger and thus is converted to allantoin. Increased allantoin levels suggest the possible involvement of free radicals in rheumatoid arthritis.
Increased kynurenine/tryptophan-reflects trytophan degradation-and neopterin levels have been regarded as a biochemical marker of cell-mediated immune response and inflammation. This study was designed to evaluate the usefulness of tryptophan degradation and neopterin levels in active rheumatoid arthritis patients under therapy. In this case-control study, kynurenine and tryptophan levels were determined by HPLC; neopterin and tumor necrosis factor-α levels were measured with ELISA in 32 active rheumatoid arthritis patients and 20 healthy controls. Although mean values of tryptophan, kynurenine, ratio of kynurenine to tryptophan, neopterin, and tumor necrosis factor-α levels did not show statistically significant differences between patient and control groups, neopterin levels correlated positively with kynurenine (r = 0.582, p < 0.02), kynurenine/tryptophan (r = 0.486, p < 0.05), erythrocyte sedimentation rate (r = 0.472, p < 0.05) and RF (r = 0.478, p < 0.05) in the rheumatoid arthritis group. CRP levels of the patient group correlated with kynurenine levels (r = 0.524, p < 0.03). Determination of tryptophan degradation and neopterin levels in chronic inflammatory disease may provide a better understanding of progression of the disease.
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