Helicobacter pylori
infection is responsible for
inflammation, increased production of
reactive oxygen species 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
reactive oxygen species 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 high performance liquid chromatography prepurification/gas chromatography with
isotope dilution mass detection methodology, we examined the amount of oxidatively damaged
DNA products excreted into urine and the amount of
8-oxodG in the
DNA of leukocytes' (with the the 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
nitric oxide mediated inhibition of a key base excision repair
enzyme (human 8-oxo-7, 8-dihydroguanine glycosylase) responsible for the repair of
8-oxo-7,8-dihydroguanine.