Abstract
Telomere shortening during human aging has been reported to be accelerated by oxidative stress. We investigated the mechanism of telomere shortening by oxidative stress. H 2O 2 plus Cu(II) caused predominant DNA damage at the 5′ site of 5′-GGG-3′ in the telomere sequence. Furthermore, H 2O 2 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.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call