Telomeres undergo a progressive shortening process as individuals age, and it has been proposed that severely shortened and dysfunctional telomeres play a role in the aging process and the onset of age-related diseases in human beings. An emerging body of evidence indicates that the shortening of telomeres in cultured human cells is also influenced by other replication defects occurring within telomeric repeats. These abnormalities can be detected on metaphase chromosomes. Recent studies have also identified a set of serological markers for telomere dysfunction and DNA damage (elongation factor 1α [EF-1α], stathmin, and N-acetyl-glucosaminidase). With this study, the correlation between telomere abnormalities (by FISH) and these biomarkers as measured in blood serum (by ELISA) from a cohort of 22 healthy subjects at different ages (range 26–101 years) was analyzed. A strong positive correlation between aging and the presence of aberrant telomere structures, sister telomere loss (STL), and sister telomere chromatid fusions (STCF) was detected. When serum markers of telomere dysfunction were correlated with telomere abnormalities, we found that stathmin correlated with total aberrant telomeres structures (r = 0.431, p = 0.0453) and STCF (r = 0.533, p = 0.0107). These findings suggest that serum stathmin can be considered an easy-to-get marker of telomere dysfunction and may serve as valuable indicators of aging.

随着个体年龄的增长，端粒会经历一个逐渐缩短的过程，有人提出，严重缩短和功能失调的端粒在人类衰老过程和与年龄相关的疾病的发作中发挥作用。新出现的证据表明，培养的人类细胞中端粒的缩短也受到端粒重复序列中发生的其他复制缺陷的影响。这些异常可以在中期染色体上检测到。最近的研究还确定了一组端粒功能障碍和 DNA 损伤的血清学标志物（延伸因子 1α [EF-1α]、stathmin 和 N-乙酰氨基葡萄糖苷酶）。通过这项研究，分析了端粒异常（通过 FISH）与来自一组 22 名不同年龄（范围 26-101 岁）的健康受试者的血清（通过 ELISA）中测量的这些生物标志物之间的相关性。检测到衰老与异常端粒结构、姐妹端粒丢失 （STL） 和姐妹端粒染色单体融合 （STCF） 之间存在很强的正相关。当端粒功能障碍的血清标志物与端粒异常相关时，我们发现 stathmin 与总异常端粒结构 （r = 0.431，p = 0.0453） 和 STCF （r = 0.533，p = 0.0107） 相关。这些发现表明，血清 stathmin 可以被认为是端粒功能障碍的容易获得的标志物，并可能作为有价值的衰老指标。