Site-specific DNA damage at GGG sequence by oxidative stress may accelerate telomere shortening
Site-specific DNA damage at GGG sequence by oxidative stress may accelerate telomere shortening
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DOI：
10.1016/s0014-5793(99)00748-6
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发表时间：
1999-06-25
期刊：
影响因子：
3.5
通讯作者：
Kawanishi, S
中科院分区：
文献类型：
--
作者：
Oikawa, S;Kawanishi, S
据报道，氧化应激加速了人类衰老过程中端粒的缩短。我们研究了氧化应激导致端粒缩短的机制。H_2O_2 + Cu（Ⅱ）对端粒序列中5 ′-GGG-3 ′的5 ′位点的DNA损伤占优势。此外，H_2O_2 + Cu（II）诱导端粒序列中8-oxo-7，8-dihydro-2 '-deoxyguanosine（8-oxodG）的形成比非端粒序列中更有效。NO + O-2（-）能有效地引起端粒序列中5 ′-GGG-3 ′ 5 ′位点的碱基改变。因此，氧化应激对GGG序列的DNA损伤可能是导致端粒缩短的重要因素。(C)1999年欧洲生物化学学会联合会。
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.