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Carcinogenesis Advance Access published online on October 11, 2005
Carcinogenesis, doi:10.1093/carcin/bgi238
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received July 15, 2005
Revised September 9, 2005
Accepted September 28, 2005

CANCER BIOLOGY

Helicobacter pylori infection is associated with oxidatively damaged DNA in human leukocytes and decreased level of urinary 8-oxo-7,8-dihydroguanine

Agnieszka Siomek 1, Agnieszka Rytarowska 2, Anna Szaflarska-Poplawska 2, Daniel Gackowski 1, Rafal Rozalski 1, Tomasz Dziaman 1, Mieczyslawa Czerwionka-Szaflarska 2, and Ryszard Olinski 1*

1 Department of Clinical Biochemistry, Nicolaus Copernicus University, Collegium Medicum in Bydgoszcz, Karlowicza 24, 85-092 Poland
2 Chair and Dapartment of Pediatrics, Allergology and Gastroenterology, Nicolaus Copernicus University, Collegium Medicum in Bydgoszcz, Curie-Sklodowskiej 9, 85-094 Poland

* To whom correspondence should be addressed.
Ryszard Olinski, E-mail: ryszardo{at}cm.umk.pl


  Abstract

H.pylori infection is responsible for inflammation, increased production of reactive oxygen species (ROS) and oxidatively damaged DNA in the gastric mucosa. There is also evidence which suggests that H.pylori infection may lead to the development of several extragastroduodenal pathologies with ROS involvement. In order to assess whether the infection may impose oxidatively damaged DNA not only in the target organ (stomach) but in other organs as well we decided, for the first time, to analyse the two kinds of oxidatively damaged DNA biomarkers: urinary excretion of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) and 8-oxo-7,8-dihydroguanine (8-oxoGua) as well as the level of oxidatively damaged DNA in leukocytes. Using HPLC prepurification/isotope dilution GC/MS methodology, we examined the amount of oxidatively damaged DNA products excreted into urine and the amount of 8-oxodG in leukocytes' DNA (with HPLC/EC technique) in three groups of children: i/ control group, ii/ H.pylori infected children and iii/ children with gastritis where H.pylori infection was excluded. The levels of 8-oxodG in DNA isolated from leukocytes of H.pylori infected patients and in the group with gastritis without H.pylori infection were significantly higher than in DNA isolated from the control group. The mean level of 8-oxoGua in urine samples of children infected with H.pylori was significantly lower than in the urine of the group with gastritis without H.pylori infection. The data suggest that inflammation itself not just H.pylori infection is responsible for the observed rise of 8-oxodG level in leukocytes. However, the observed decrease in the level of modified base in urine seems to be specific for H.pylori infection and possibly linked with NO mediated inhibition of a key base excision repair enzyme (hOGG1) responsible for repair of 8-oxo-7,8-dihydroguanine.


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