Site-specific DNA damage at GGG sequence by oxidative stress may accelerate telomere shortening

被引：318

作者：

Oikawa, S ^{[1
]}

Kawanishi, S ^{[1
]}

机构：

[1] Mie Univ, Sch Med, Dept Hyg, Mie 5148507, Japan

来源：

FEBS LETTERS | 1999年 / 453卷 / 03期

关键词：

DNA damage; telomere; aging; hydrogen peroxide; nitric oxide;

D O I：

10.1016/S0014-5793(99)00748-6

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Telomere shortening during human aging has been reported to be accelerated by oxidative stress. We investigated the mechanism of telomere shortening by oxidative stress. H2O2 plus Cu(II) caused predominant DNA damage at the 5' site of 5'-GGG-3' in the telomere sequence. Furthermore, H2O2 plus Cu(II) induced 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) formation in telomere sequences more efficiently than that in non-telomere sequences. NO plus O-2(-) efficiently caused base alteration at the 5' site of 5'-GGG-3' in the telomere sequence. It is concluded that the site-specific DNA damage at the GGG sequence by oxidative stress may play an important role in increasing the rate of telomere shortening with aging. (C) 1999 Federation of European Biochemical Societies.

引用

页码：365 / 368

页数：4

共 47 条

[1] TELOMERE LENGTH PREDICTS REPLICATIVE CAPACITY OF HUMAN FIBROBLASTS [J].