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Site‐specific DNA damage at GGG sequence by oxidative stress may accelerate telomere shortening
Author(s) -
Oikawa Shinji,
Kawanishi Shosuke
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00748-6
Subject(s) - telomere , oxidative stress , dna , sequence (biology) , dna damage , deoxyguanosine , chemistry , base pair , senescence , biophysics , microbiology and biotechnology , biology , biochemistry , genetics
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 2 O 2 plus Cu(II) caused predominant DNA damage at the 5′ site of 5′‐GGG‐3′ in the telomere sequence. Furthermore, H 2 O 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.