Human gastric diseases have shown significant changes in the activity and expression of superoxide dismutase (SOD) isoforms. The aim of this study was to detect Mn-SOD activity and expression in the tissue of gastric mucosa, primarily in chronic gastritis (immunohistochemical Helicobacter pylori-negative gastritis, without other pathohistological changes) and to evaluate their possible connection with pathohistological diagnosis. We examined 51 consecutive outpatients undergoing endoscopy for upper gastrointestinal symptoms. Patients were classified based on their histopathological examinations and divided into three groups: 51 patients (archive samples between 2004-2009) with chronic immunohistochemical Helicobacter pylori-negative gastritis (mononuclear cells infiltration were graded as absent, moderate, severe) divided into three groups. Severity of gastritis was graded according to the updated Sydney system. Gastric tissue samples were used to determine the expression of Mn-SOD with anti-Mn-SOD Ab immunohistochemically. The Mn-SOD expression was more frequently present in specimens with severe and moderate inflammation of gastric mucosa than in those with normal mucosa. In patients with normal histological finding, positive immunoreactivity of Mn-SOD was not found. Our results determine the changes in Mn-SOD expression occurring in the normal gastric mucosa that had undergone changes in the intensity of chronic inflammatory infiltrates in the lamina propria.

Host intracellular iron has been recognized as an important cofactor in induction of nicotinamide adenine dinucleotide phosphate (NADPH)-dependent oxidative burst as antimicrobial defense mechanism. It is plausible that iron chelator directly inactivates NADPH oxidase by chelating the active site heme iron of flavocytochrome b558 thus blocking the transfer of electrons from NADPH to oxygen and its reduction to superoxide anion. Thus, altering the equilibrium of intracellular iron could influence the course of infection to the enhancement of the pathogen with regard to oxidative stress.

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A number of study have suggested a relationship between Helicobacter pylori infection and oxidative stress in the gastric epithelium. The oxidant- induced changes in zinc, iron, and vitamin C increase susceptibility to oxidative injury. Understanding of pathophysiologic mechanisms may provide new therapeutic strategies in treatment of oxidative injury of mucosa.