Chronically ultraviolet-exposed human skin shows a higher mutation frequency of mitochondrial DNA as compared to unexposed skin and the hematopoietic system
Chronically ultraviolet-exposed human skin shows a higher mutation frequency of mitochondrial DNA as compared to unexposed skin and the hematopoietic system
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DOI：
10.1111/j.1751-1097.1997.tb08654.x
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发表时间：
1997-08-01
影响因子：
3.3
通讯作者：
Krutmann, J
中科院分区：
文献类型：
--
作者：
Berneburg, M;Gattermann, N;Krutmann, J
正常的衰老过程与线粒体（mt） DNA内突变的积累有关，最常见的突变是4977碱基对（bp）的缺失，称为常见缺失。为了验证长期暴露在阳光下的皮肤以mtDNA突变频率增加为特征的假设，在同一个体中，比较了皮肤和另一个复制组织（造血系统）之间常见缺失的突变频率，以及长期暴露于阳光下与阳光保护下的皮肤，这是通过使用半定量聚合酶链反应方法比较同一标本中突变mtDNA分子与整个线粒体基因组的数量来完成的，从而允许直接比较不同组织。在所有皮肤样本中都可以观察到共同缺失，相比之下，10个血液样本中只有3个显示出可检测到的共同缺失量，晒伤皮肤与晒伤皮肤的比较显示，晒伤皮肤中有7个人的共同缺失含量更高，此外，迄今为止未描述的mtDNA突变仅在人类皮肤中检测到。这些研究表明，人类皮肤暴露在太阳辐射下可能通过氧化损伤导致mtDNA突变的积累，这可能在光老化中起重要作用。
Normal ageing processes are associated with an accumulation of mutations within the mitochondrial (mt) DNA, The most frequent mutation is a 4977 base pair (bp) deletion known as common deletion, In order to test the hypothesis that chronically sun-exposed skin is characterized by an increased mutation frequency of mtDNA, the mutation frequency of the common deletion between skin and another replicating tissue (the hematopoietic system) and chronically sun-exposed versus sun-protected skin was compared in the same individuals, This was done by comparing the amount of mutated mtDNA molecules with the whole mitochondrial genome in the same specimen with a semiquantitative polymerase chain reation method, thus allowing direct comparison of different tissues. In all skin specimens the common deletion could be observed, In contrast only 3 of 10 blood samples revealed detectable amounts of the common deletion, Comparison of sun-exposed versus sun-protected skin exhibited a higher content of the common deletion in sun-exposed skin in 7 of 10 individuals, Additionally, a hitherto undescribed mtDNA mutation was detected exclusively in human skin, These studies indicate that exposure of human skin to solar radiation leads to an accumulation of mtDNA mutations, possibly via oxidative damage, which may play an important role in photoageing.