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It has been suggested that the free radicals are closely related with peptic ulcer disease and gastritis. Although many studies have been undertaken to clarify the role of oxygen-derived free radicals, most of them were carried out in animal models. The aim of this study was to assess the reactive oxygen species activity and the damage in Helicobacter pyloriinfected gastric mucosa in humans.

In a total group of 42, there were fifteen cases of peptic ulcer, 14 cases of gastritis and 12 control subjects. Measurement of gastric mucosal malondialdehyde concentrations, which is the end - product of lipid peroxidation, was used to assess oxidative damage to membranes in patients with peptic ulcer and gastritis. Mucosal reduced glutathione glutathione concentrations were also measured in order to study whether reactive oxygen species generation affects levels of the antioxidant peptide, malondialdehyde and glutathione content was then measured in biopsies taken from the gastric antrum.

Tissue levels of glutathione were significantly (p <0.001) and malondialdehyde was higher (p<0.001) in patients with peptic ulcer compared to controls. In patients with gastritis, glutathione was also lower (p<0.001) and malondialdehyde higher (p<0.01).

Depletion of gastric mucosal glutathione in cases with H.pylori positive peptic ulcer and gastritis may be caused by accumulation of free radicals that can initiate membrane damage by lipid peroxidation.