白癜风患者线粒体DNA拷贝数水平升高。
Increased levels of mitochondrial DNA copy number in patients with vitiligo.
作者信息
Vaseghi H, Houshmand M, Jadali Z
机构信息
Department of Biology, Faculty of Biological Sciences, Gonbad Kavous University, Gonbad Kavous, Iran.
Medical Genetics Department, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran.
出版信息
Clin Exp Dermatol. 2017 Oct;42(7):749-754. doi: 10.1111/ced.13185. Epub 2017 Sep 3.
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.
背景
已知氧化应激参与白癜风等自身免疫性疾病的发病机制。有证据表明，人类线粒体DNA拷贝数（mtDNAcn）易受氧化应激介导的损伤。本研究的目的是检测和比较白癜风患者与健康对照者（HCs）外周血mtDNAcn和氧化性DNA损伤副产物（8-羟基-2'-脱氧鸟苷；8-OHdG）。
方法
通过实时定量PCR测定每个样本的相对mtDNAcn和氧化损伤（mtDNA中8-OHdG的形成）。从56例白癜风患者和46例健康对照者获取血样。
结果
白癜风患者的平均mtDNAcn和mtDNA损伤程度高于健康对照者。
结论
这些数据表明，mtDNAcn增加和氧化性DNA损伤可能参与白癜风的发病机制。
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