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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >DNA damage and repair in telomeres: relation to aging.
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DNA damage and repair in telomeres: relation to aging.

机译：端粒中的DNA损伤和修复：与衰老有关。

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摘要

We have established a method for the detection of DNA damage and its repair in human telomeres, the natural ends of chromosomes which are necessary for replication and critical for chromosomal stability. We find that ultraviolet light-induced pyrimidine dimers in telomeric DNA are repaired less efficiently than endogenous genes but more efficiently than inactive, noncoding regions. We have also measured telomeric length, telomeric DNA damage, and its repair in relation to the progression of aging. Telomeres are shorter in fibroblasts from an old donor compared to fibroblasts from a young donor, shortest in cells from a patient with the progeroid disorder Werner syndrome, and relatively long in fibroblasts from a patient with Alzheimer disease. Telomeric DNA repair efficiency is lower in cells from an old donor than in cells from a young donor, normal in Alzheimer cells, and slightly lower in Werner cells. It is possible that this decline in telomeric repair with aging is of functional significance to an age-related decline in genomic stability.
机译：我们已经建立了一种检测人类端粒中DNA损伤及其修复的方法，端粒是复制所必需的染色体的天然末端，对于染色体的稳定性至关重要。我们发现端粒DNA中的紫外线诱导的嘧啶二聚体比内源性基因修复效率低，但比非活性非编码区修复效率更高。我们还测量了端粒长度，端粒DNA损伤及其与衰老进程相关的修复。与来自年轻供体的成纤维细胞相比，来自老年供体的成纤维细胞更短，在患有早衰症沃纳综合症患者的细胞中，端粒最短，而来自阿尔茨海默病患者的成纤维细胞则相对较长。老年供体的细胞端粒DNA修复效率比年轻供体的细胞低，阿尔茨海默细胞正常，而维尔纳细胞则低。随着年龄的增长，端粒修复的下降可能与年龄相关的基因组稳定性下降具有功能上的意义。

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