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DNA damage in human respiratory tract epithelial cells: damage by gas phase cigarette smoke apparently involves attack by reactive nitrogen species in addition to oxygen radicals
Author(s) -
Spencer Jeremy P.E,
Jenner Andrew,
Chimel Ken,
Aruoma Okezie I,
Cross Carroll E,
Wu Reen,
Halliwell Barry
Publication year - 1995
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 - 10.1016/0014-5793(95)01199-o
Subject(s) - dna damage , chemistry , reactive oxygen species , radical , respiratory tract , deamination , dna , guanine , xanthine , oxygen , hypoxanthine , cigarette smoke , reactive nitrogen species , photochemistry , biochemistry , respiratory system , biology , organic chemistry , toxicology , enzyme , anatomy , nucleotide , gene
Treatment of human respiratory tract tracheobronchial epithelial cells with gas‐phase cigarette smoke led to dose‐dependent DNA strand breakage that was highly correlated with multiple chemical modifications of all four DNA bases. The pattern of base damage suggests attack by hydroxyl radicals (OH : ). However, by far the most important base damage in quantitative terms was formation of xanthine and hypoxanthine, presumably resulting from deamination of guanine and adenine respectively. Hence, DNA damage by cigarette smoke may involve reactive nitrogen species as well as reactive oxygen species.