Abstract

Objective
 Oxidative stress has been shown to play a role in the pathophysiology of several diseases, making it a popular yet contentious research area. There is some evidence that selective melanocyte destruction may have developed in vitiligo patients as a result of elevated oxidative stress. The purpose of this study is to investigate the impact of oxidative stress on lipid, protein, and nucleic acid metabolism in vitiligo patients.
 Method
 We used ELISA method to measure serum oxidative stress markers in patients with generalized vitiligo who had newly formed lesions in the previous three months but had not been treated, as well as healthy controls. Malondialdehyde (MDA), 2,4-dinitrophenyl hydrazone (DNPH), 8-hydroxy-2'-deoxyguanosine (8-OHdG), and uncoupling protein 2 (UCP2) levels were measured to assess the influence of reactive oxygen derivatives on lipid, protein, nucleic acid metabolism, and mitochondria, respectively. 
 Results
 The study included 84 participants, including 64 active generalized vitiligo patients and 20 healthy controls with similar age and gender distribution. In the serum of vitiligo patients, we detected significantly lower levels of MDA (ng/mL, mean±SD=12±19; 33.4±35.9), DNPH (ng/mL, mean±SD=2±3.1; 6±7.4), 8-OHdG (ng/mL, mean±SD=11.7±17.9; 32.7±37) and UCP2 (ng/mL, mean±SD=8.7±13.7; 21.5±28.4).
 
 Conclusion
 Although there is significant evidence that oxidative stress plays a role in the pathophysiology of vitiligo, the studies should be interpreted cautiously due to the heterogeneity in the methodology, complexity of the oxidative stress pathways, and potential publication bias. Large-scale studies using a standardized methodology are required to determine how significant oxidative stress is in the core pathophysiology of vitiligo and which pathways it primarily affects.

Full Text
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