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Oxidative stress, telomere length and biomarkers of physical aging in a cohort aged 79 years from the 1932 Scottish Mental Survey.
Mechanisms of Ageing and Development ( IF 5.3 ) Pub Date : 2008-10-14 , DOI: 10.1016/j.mad.2008.09.020
John M Starr 1 , Paul G Shiels , Sarah E Harris , Alison Pattie , Mark S Pearce , Caroline L Relton , Ian J Deary
Affiliation  

Telomere shortening is a biomarker of cellular senescence and is associated with a wide range of age-related disease. Oxidative stress is also associated with physiological aging and several age-related diseases. Non-human studies suggest that variants in oxidative stress genes may contribute to both telomere shortening and biological aging. We sought to test whether oxidative stress-related gene polymorphisms contribute to variance in both telomere length and physical biomarkers of aging in humans. Telomere lengths were calculated for 190 (82 men, 108 women) participants aged 79 years and associations with 384 SNPs, from 141 oxidative stress genes, identified 9 significant SNPS, of which those from 5 genes (GSTZ1, MSRA, NDUFA3, NDUFA8, VIM) had robust associations with physical aging biomarkers, respiratory function or grip strength. Replication of associations in a sample of 318 (120 males, 198 females) participants aged 50 years confirmed significant associations for two of the five SNPs (MSRA rs4841322, p=0.008; NDUFA8 rs6822, p=0.048) on telomere length. These data indicate that oxidative stress genes may be involved in pathways that lead to both telomere shortening and physiological aging in humans. Oxidative stress may explain, at least in part, associations between telomere shortening and physiological aging.

中文翻译:

来自 1932 年苏格兰心理调查的 79 岁队列中的氧化应激、端粒长度和身体衰老的生物标志物。

端粒缩短是细胞衰老的生物标志物,与多种年龄相关疾病有关。氧化应激还与生理衰老和几种与年龄有关的疾病有关。非人类研究表明,氧化应激基因的变异可能导致端粒缩短和生物老化。我们试图测试与氧化应激相关的基因多态性是否会导致端粒长度和人类衰老的物理生物标志物的变化。计算了 190 名 79 岁的参与者(82 名男性,108 名女性)的端粒长度,并与来自 141 个氧化应激基因的 384 个 SNP 相关,确定了 9 个重要的 SNPS,其中来自 5 个基因(GSTZ1、MSRA、NDUFA3​​、NDUFA8、VIM ) 与身体衰老生物标志物、呼吸功能或握力有密切的关联。50 岁的 318 名(120 名男性,198 名女性)参与者样本中的关联复制证实了五个 SNP 中的两个(MSRA rs4841322,p=0.008;NDUFA8 rs6822,p=0.048)与端粒长度的显着关联。这些数据表明,氧化应激基因可能参与导致人类端粒缩短和生理衰老的途径。氧化应激至少可以部分解释端粒缩短与生理衰老之间的关联。
更新日期:2019-11-01
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