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线粒体如何以人体皮肤组织为模型记录紫外线照射和氧化应激的影响。

How mitochondria record the effects of UV exposure and oxidative stress using human skin as a model tissue.

机构信息

Department of Dermatological Sciences, Institute of Cellular Medicine, Medical School, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.

出版信息

Mutagenesis. 2010 Mar;25(2):101-7. doi: 10.1093/mutage/gep061. Epub 2009 Dec 2.

DOI:10.1093/mutage/gep061
PMID:19955330
Abstract

The accumulation of mitochondrial DNA (mtDNA) mutations has been proposed as an underlying cause of the ageing process and mutations have been associated with cancer in many tissues, including human skin. This involvement is linked to the key roles of mitochondrial function and mtDNA in oxidative stress production and as a mediator of apoptosis. We and others have pioneered the use of mtDNA damage as a highly sensitive biomarker of ultraviolet exposure in human skin and have also shown that the accumulation of an ageing-dependent mtDNA mutation is accelerated by exposure to sunlight, which is known to induce oxidative stress in skin. This is important as ultraviolet radiation (UVR)-induced gene mutations play a key role in the development of skin cancer and ageing in human skin. Novel applications of mtDNA as a biomarker of UVR-induced oxidative stress will also be highlighted in this review.

摘要

线粒体 DNA(mtDNA)突变的积累被认为是衰老过程的潜在原因,并且在许多组织中,包括人类皮肤,突变与癌症有关。这种参与与线粒体功能和 mtDNA 在氧化应激产生中的关键作用以及作为细胞凋亡的介质有关。我们和其他人开创了使用 mtDNA 损伤作为人类皮肤紫外线暴露的高度敏感生物标志物的先河,并且还表明,暴露于阳光会加速与年龄相关的 mtDNA 突变的积累,众所周知,阳光会在皮肤中引起氧化应激。这很重要,因为紫外线辐射(UVR)诱导的基因突变在人类皮肤癌和衰老的发展中起着关键作用。本综述还将重点介绍 mtDNA 作为 UVR 诱导的氧化应激生物标志物的新应用。

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