An investigation of mutation as a function of age in humans

C.M. King, E.S. Gillespie, P.G. McKenna, Y.A. Barnett
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引用次数: 82

Abstract

An accumulation of mutations on their own or together with other age-related changes may contribute to ageing and the development of age-related pathologies. The aim of this investigation wass to assess the extent of DNA mutations as a function of age in humans. The mutant frequency (MF) at the hypoxanthine-guanine phosphoribosyl-transferase (hgprt) locus was assessed in lymphocytes isolated from male volunteers in each of three age groups (35–39, 50–54 and 65–69 years). Results show that the mean MF in the 65–69 years group was approximately twice that in the 35–39 and 50–54 years (4.1/106 cells, 1.9/106 cells and 1.79/106 cells, respectively) increasingly by about 1.33% per year, after 54 years. In addition, there was an increased frequency of chromosomal aberrations in the 65–69 years group compared to the other two age groups. The results of this investigation show an increase in DNA mutations in cultured human lymphocytes with age. Factors which may influence the extent of DNA damage in human lymphocytes are discussed.

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对人类年龄变化的研究
突变本身的积累或与其他与年龄相关的变化一起可能导致衰老和与年龄相关的病理的发展。这项研究的目的是评估人类DNA突变随年龄变化的程度。在三个年龄组(35-39岁、50-54岁和65-69岁)的男性志愿者中分离的淋巴细胞中,评估了次黄嘌呤-鸟嘌呤磷酸酰基转移酶(hgprt)位点的突变频率(MF)。结果表明,65-69岁组平均MF约为35-39岁和50-54岁组的2倍(分别为4.1/106、1.9/106和1.79/106),54年后以每年约1.33%的速度递增。此外,与其他两个年龄组相比,65-69岁年龄组的染色体畸变频率增加。这项研究的结果表明,随着年龄的增长,培养的人类淋巴细胞中的DNA突变增加。讨论了可能影响人淋巴细胞DNA损伤程度的因素。
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Publisher's note Editorial An accessory protein enhances both DNA binding and activity of DNA polymerase α isolated from normal, but not transformed, human fibroblasts Differences in the spectrum of spontaneous mutations in the hprt gene between tumor cells of the microsatellite mutator phenotype Spermatid micronucleus analysis of aging effects in hamsters
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