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

Alfredo Papa, S. Danese, A. Sgambato, R. Ardito, G. Zannoni, A. Rinelli, F. M. Vecchio, N. Gentiloni-Silveri, A. Cittadini, G. Gasbarrini, A. Gasbarrini

Research output: Contribution to journalArticle

Abstract

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 I 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-tree radicals-mediated damage due to H. pylori cytotoxic strains could be a driving force that leads from chronic gastritis to gastric carcinoma.

Original languageEnglish
Pages (from-to)409-413
Number of pages5
JournalScandinavian Journal of Gastroenterology
Volume37
Issue number4
DOIs
Publication statusPublished - 2002

Fingerprint

Gastric Mucosa
Helicobacter pylori
DNA Damage
Reactive Oxygen Species
Infection
Genes
Helicobacter Infections
Stomach
Luminol
Gastritis
Luminescence
Stomach Neoplasms
Carcinogenesis
Monoclonal Antibodies
Bacteria
Carcinoma
Biopsy
Neoplasms

Keywords

  • 8-hydroxy-2′-deoxyguanosine
  • Cancerogenesis
  • Cytotoxic associated gene A
  • Helicobacter pylori
  • Reactive oxygen species

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Role of Helicobacter pylori CagA+ infection in determining oxidative DNA damage in gastric mucosa. / Papa, Alfredo; Danese, S.; Sgambato, A.; Ardito, R.; Zannoni, G.; Rinelli, A.; Vecchio, F. M.; Gentiloni-Silveri, N.; Cittadini, A.; Gasbarrini, G.; Gasbarrini, A.

In: Scandinavian Journal of Gastroenterology, Vol. 37, No. 4, 2002, p. 409-413.

Research output: Contribution to journalArticle

Papa, A, Danese, S, Sgambato, A, Ardito, R, Zannoni, G, Rinelli, A, Vecchio, FM, Gentiloni-Silveri, N, Cittadini, A, Gasbarrini, G & Gasbarrini, A 2002, 'Role of Helicobacter pylori CagA+ infection in determining oxidative DNA damage in gastric mucosa', Scandinavian Journal of Gastroenterology, vol. 37, no. 4, pp. 409-413. https://doi.org/10.1080/003655202317316033
Papa, Alfredo ; Danese, S. ; Sgambato, A. ; Ardito, R. ; Zannoni, G. ; Rinelli, A. ; Vecchio, F. M. ; Gentiloni-Silveri, N. ; Cittadini, A. ; Gasbarrini, G. ; Gasbarrini, A. / Role of Helicobacter pylori CagA+ infection in determining oxidative DNA damage in gastric mucosa. In: Scandinavian Journal of Gastroenterology. 2002 ; Vol. 37, No. 4. pp. 409-413.
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abstract = "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 I 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-tree radicals-mediated damage due to H. pylori cytotoxic strains could be a driving force that leads from chronic gastritis to gastric carcinoma.",
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AU - Papa, Alfredo

AU - Danese, S.

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AU - Ardito, R.

AU - Zannoni, G.

AU - Rinelli, A.

AU - Vecchio, F. M.

AU - Gentiloni-Silveri, N.

AU - Cittadini, A.

AU - Gasbarrini, G.

AU - Gasbarrini, A.

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N2 - 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 I 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-tree radicals-mediated damage due to H. pylori cytotoxic strains could be a driving force that leads from chronic gastritis to gastric carcinoma.

AB - 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 I 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-tree radicals-mediated damage due to H. pylori cytotoxic strains could be a driving force that leads from chronic gastritis to gastric carcinoma.

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