Background: Helicobacter pylori (HP) is the main pathogenic factor in the development of gastritis and gastric cancer. Superoxide-dismutase (SOD) is a key enzyme of mucosal antioxidant protection. In the presence of HP there is a significant increase of SOD activity in the antrum. Changes in gastric mucosal SOD activity were detected in response to eradication treatment of HP infection.
Patients And Methods: Biopsies were taken from 13 patients upon gastroscopy performed prior to and 88.3 +/- 12.6 days after treatment. The activity of SOD was determined by spectrophotometry.
Results: The activity of SOD in the gastric mucosa decreased significantly following the successful eradication, whereas in the corpus activity did not change significantly.
Conclusion: In the presence of HP there is an oxidative stress in the gastric mucosa triggered by the bacterium. It may represent the final common path of HP carcinogenesis. Successful eradication treatment prevents the production of reactive oxygen metabolites.
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