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

FEBS Letters

Wu, Reen²  Aruoma, Okezie I³  Jenner, Andrew³  Cross, Carroll E¹  Halliwell, Barry³  Spencer, Jeremy P.E³  Chimel, Ken² 

[1] Division of Pulmonary/Critical Care Medicine, Department of Internal Medicine, UC Davis Medical Centre, Sacramento, California, 95817, USA;Pulmonary Research Group, Californian Regional Primate Research Centre, UC Davis, Davis, California, 95616, USA;Neurodegenerative Disease Research Centre, University of London King's College, Manresa Road, London, SW3 6LX, UK

关键词: Human respiratory tract cell;    DNA damage;    DNA base modification;    Strand breakage;    Cigarette smoke;    GC-MS;    5-OH-uracil;    5-hydroxyuracil;    5-OHMe-uracil;    5-(hydroxymethyl)uracil;    FAPy-adenine;    4;    6-diamino-5-formamidopyrimidine;    8-OH-adenine;    8-hydroxyadenine;    FAPy-guanine;    2;    6-diamino-4-hydroxy-5-formamidopyrimidine;    8-OH-guanine;    8-hydroxyguanine;    8OHdG;    8-hydroxy-2′-deoxyguanosine;   

DOI  :  10.1016/0014-5793(95)01199-O

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown