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.

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.

DNA strand breakage and base modification induced by hydrogen peroxide treatment of human respiratory tract epithelial cells.

Treatment of human respiratory tract epithelial cells with H2O2 led to concentration-dependent DNA strand breakage that was highly-correlated with multiple chemical modifications of all four DNA bases, suggesting that damage is due to hydroxyl radical, OH. However, the major base damage occurred to adenine. Hence, conclusions made about the occurrence and the extent of oxidative DNA damage on the basis only of changes in 8-hydroxyguanine should be approached with caution.