Site-specific DNA damage at GGG sequence by oxidative stress may accelerate telomere shortening.
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 O2- 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.
Department of Hygiene, Mie University School of Medicine, Japan.
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Oikawa
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Kawanishi
D001483:Base Sequence; D003300:Copper / Q000494:pharmacology; D004249:DNA Damage; D003848:Deoxyguanine Nucleotides / Q000378:metabolism*; D003849:Deoxyguanosine / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000494:pharmacology; D006900:Hydroxylation; D008981:Molsidomine / Q000031:analogs & derivatives / Q000494:pharmacology; D009841:Oligonucleotides / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D016615:Telomere / Q000502:physiology*
D003848:Deoxyguanine Nucleotides; D009841:Oligonucleotides; C002385:linsidomine; D003300:Copper; D006861:Hydrogen Peroxide; D008981:Molsidomine; D003849:Deoxyguanosine