Role of Helicobacter pylori CagA+ infection in determining oxidative DNA damage in gastric mucosa

Antonio Gasbarrini, Alfredo Papa, S Danese, Alessandro Sgambato, R Ardito, Gian Franco Zannoni, A Rinelli, Fm Vecchio, N Gentiloni Silveri, A Cittadini, G. Gasbarrini

Risultato della ricerca: Contributo in rivistaArticolo in rivista


BACKGROUND: Although Helicobacter pylori is a risk factor for gastric cancer, the role of the bacterium in the development of this malignancy is not defined precisely. Reactive oxygen species (ROS) could play an important role in carcinogenesis by inducing DNA damage. The aims of the present study were: 1) to assess the production of ROS and 8-hydroxy-2'-deoxyguanosine (8-OHdG), a sensitive marker of oxidative DNA injury, in gastric mucosa, according to H. pylori status and cytotoxic associated gene product A (CagA); 2) to determine the relationship between ROS generation and amount of 8-OHdG. METHODS: Gastric biopsy specimens were obtained from 60 consecutive patients. ROS generation was measured by luminol enhanced chemiluminescence. 8-OHdG detection was performed by an immunoperoxidase method, using a specific anti 8-OHdG monoclonal antibody. RESULTS: 40/60 patients (67%) were H. pylori-positive. ROS generation was significantly higher in patients positive for H. pylori infection as compared to negative. 8-OHdG detection was performed in 30 patients in which CagA presence was also investigated. High expression of 8-OHdG was detected in 14/20 (70%) H. pylori-positive patients (13 CagA+ and 1 CagA-) and in 2/10 (20%) H. pylori-negative patients. A significant correlation was found between ROS production and 8-OHdG content. CONCLUSION: H. pylori infection by a CagA+ strain is associated with the highest production of ROS to which a severe oxidative DNA damage corresponds. This sequence of events could support the hypothesis that the oxygen-free radicals-mediated damage due to H. pylori cytotoxic strains could be a driving force that leads from chronic gastritis to gastric carcinoma.
Lingua originaleEnglish
pagine (da-a)409-413
Numero di pagine5
RivistaScandinavian Journal of Gastroenterology
Stato di pubblicazionePubblicato - 2002


  • helicobacter pylori
  • oxidative Dna damage


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