H Vaseghi1, M Houshmand2, Z Jadali3. 1. Department of Biology, Faculty of Biological Sciences, Gonbad Kavous University, Gonbad Kavous, Iran. 2. Medical Genetics Department, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran. 3. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Abstract
BACKGROUND: Oxidative stress is known to be involved in the pathogenesis of autoimmune diseases such as vitiligo. Evidence suggests that the human mitochondrial DNA copy number (mtDNAcn) is vulnerable to damage mediated by oxidative stress. The purpose of this study was to examine and compare peripheral blood mtDNAcn and oxidative DNA damage byproducts (8-hydroxy-2-deoxyguanosine; 8-OHdG) in patients with vitiligo and healthy controls (HCs). METHODS: The relative mtDNAcn and the oxidative damage (formation of 8-OHdG in mtDNA) of each sample were determined by real-time quantitative PCR. Blood samples were obtained from 56 patients with vitiligo and 46 HCs. RESULTS: The mean mtDNAcn and the degree of mtDNA damage were higher in patients with vitiligo than in HCs. CONCLUSION: These data suggest that increase in mtDNAcn and oxidative DNA damage may be involved in the pathogenesis of vitiligo.
BACKGROUND: Oxidative stress is known to be involved in the pathogenesis of autoimmune diseases such as vitiligo. Evidence suggests that the human mitochondrial DNA copy number (mtDNAcn) is vulnerable to damage mediated by oxidative stress. The purpose of this study was to examine and compare peripheral blood mtDNAcn and oxidative DNA damage byproducts (8-hydroxy-2-deoxyguanosine; 8-OHdG) in patients with vitiligo and healthy controls (HCs). METHODS: The relative mtDNAcn and the oxidative damage (formation of 8-OHdG in mtDNA) of each sample were determined by real-time quantitative PCR. Blood samples were obtained from 56 patients with vitiligo and 46 HCs. RESULTS: The mean mtDNAcn and the degree of mtDNA damage were higher in patients with vitiligo than in HCs. CONCLUSION: These data suggest that increase in mtDNAcn and oxidative DNA damage may be involved in the pathogenesis of vitiligo.