Background: The pathophysiology of alopecia areata (AA) has not been clearly defined; however, it appears as a tissue-restricted autoimmune disease mediated by T lymphocytes. Immunohistochemical studies have shown peri- and infra-follicular inflammatory infiltrate which damages hair follicles. We analyzed the role of lipid peroxidation and oxidant-antioxidant enzymes in the pathogenesis of AA.
Material/methods: Twenty-four patients with AA and 20 age- and sex-matched healthy controls were enrolled in this study. We analyzed serum levels of malondialdehyde (MDA) and nitric oxide (NO) and the serum activities of superoxide dismutase (SOD) and xanthine oxidase (XO) in patients with AA and control subjects.
Results: The levels of MDA and NO (nitrite/nitrate) and the activity of XO in serum of patients with AA (0.76+/-0.34 nmol/ml, 14.88+/-6.40 nmol/ml, and 0.34+/-0.10 U/ml, respectively) were significantly higher than those of controls (0.35+/-0.09 nmol/ml, 10.71+/-1.75 nmol/ml, 0.11+/-0.03 U/ml; p<0.001, p<0.001, p<0.05, respectively). The SOD activity (12.95+/-2.16 U/ml) in the serum of patients with AA was significantly lower than that of controls (14.89+/-2.29 U/ml, p<0.05).
Conclusions: Increased lipid peroxidation in AA may be related to an increase in NO level and XO activity and a decrease in SOD activity. These results suggest that lipid peroxidation and alterations in the oxidant-antioxidant enzymatic system may play a role in the pathogenesis of AA.
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