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首页> 外文期刊>Anais Brasileiros de Dermatologia >Quantification of mitochondrial DNA damage and copy number in circulating blood of patients with systemic sclerosis by a qPCR-based assay,
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Quantification of mitochondrial DNA damage and copy number in circulating blood of patients with systemic sclerosis by a qPCR-based assay,

机译:基于QPCR的测定,通过QPCR的测定循环血液血液DNA损伤和拷贝数的定量,

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摘要

Background:Although not fully understood, oxidative stress has been implicated in the pathogenesis of different autoimmune diseases such as systemic sclerosis. Accumulating evidence indicates that oxidative stress can induce mitochondrial DNA (mtDNA) damage and variations in mtDNA copy number (mtDNAcn).Objective:The aim of this study was to explore mtDNAcn and oxidative DNA damage byproducts in peripheral blood of patients with systemic sclerosis and healthy controls.Methods:Forty six patients with systemic sclerosis and forty nine healthy subjects were studied. Quantitative real-time PCR used to measure the relative mtDNAcn and the oxidative damage (oxidized purines) of each sample.Results:The mean mtDNAcn was lower in patients with systemic sclerosis than in healthy controls whereas the degree of mtDNA damage was significantly higher in cases as compared to controls. Moreover, there was a negative correlation between mtDNAcn and oxidative DNA damage.Study limitations:The lack of simultaneous analysis and quantification of DNA oxidative damage markers in serum or urine of patients with systemic sclerosis and healthy controls.Conclusion:These data suggest that alteration in mtDNAcn and increased oxidative DNA damage may be involved in the pathogenesis of systemic sclerosis.
机译:背景:虽然尚未完全明白,但氧化应激已经涉及不同自身免疫疾病的发病机制,例如全身性硬化症。累积证据表明,氧化应激可以诱导线粒体DNA(MTDNA)损伤和MTDNA拷贝数(MTDNACN)的变化。目的:本研究的目的是探索全身硬化和健康患者外周血中的MTDNACN和氧化DNA损伤副产品对照方法:研究了四十六名患有全身硬化和四十九个健康受试者的患者。用于测量每个样品的相对mtdNAcn和氧化损伤(氧化嘌呤)的定量实时PCR,结果:系统性硬化症患者的平均mtdNAc较低,而不是健康对照,而MTDNA损伤程度明显高于病例与对照相比。此外,MTDNACN与氧化DNA损伤之间存在负相关性。研究所限制:血清中DNA氧化损伤标志物的同时分析和定量血清中的DNA氧化损伤标志物缺乏分析和定量患者患者的患者患者的血清和健康对照。结论:这些数据表明改变了MTDNACN和增加的氧化DNA损伤可能涉及系统性硬化的发病机制。

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