Superoxide dismutases in chronic gastritis

Abstract

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.

Preventive Effect of Lactobacillus Plantarum CQPC10 on Activated Carbon Induced Constipation in Institute of Cancer Research (ICR) Mice

“…The likely reason is that long-term retention and stimulation of hard faeces causes inflammation in the intestinal tract [29]. Mn-SOD can reduce the activity under inflammation [30]. SOD can transform harmful superoxide radicals into hydrogen peroxide.…”

Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

“…pylori-infected individuals with moderate to severe gastric mucosa inflammation present greater expression of Mn-SOD than individuals with the intact gastric mucosa. Mn-SOD expression was observed to be more enhanced primarily within the pit cells of the antrum and not the corpus [122]. It was reported that exposure to the CagA-positive H. pylori strains results in significantly greater SOD, catalase, and glutathione peroxidase activities compared to exposure to the CagA-negative strains [123].…”

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“…These inflammatory mediators could recruit and activate inflammatory cells, such as neutrophils and macrophages, to amplify inflammation [ 16 ]. MPO and SOD1 were involved in the oxidative stress [ 17 ]. PTGS1 and PTGS2 were related with prostaglandin, which is an important hormone in immune regulation [ 18 ].…”