Abstract

Purpose: Metallothionein (MT), a low-molecular-weight, cysteine-rich, metal-binding ligand, has proven to sequester reactive oxygen species and reduce tissue damage. Helicobacter pylori (H. pylori) infection is associated with increased production of reactive oxygen species within the gastric mucosa. This study investigates the role of MT in H. pylori-induced gastritis with or without gastric cancer and evaluates the effect on MT expression after its eradication therapy. Methods: Biopsy samples in the corpus and antrum were immunohistochemically examined for MT expression in 36 H. pylori-negative subjects without gastric cancer, and 89 positive ones with or without early gastric cancer. Gastritis was also evaluated according to an updated Sydney System. In 30 successfully eradicated subjects, the assessment described above was repeated every year for 2 years. Results: The rate of MT expression was higher in H. pylori negative subjects than in positive ones (p < 0.01). Analyzing H. pylori positive subjects, its rate was higher in those without cancer compared to cancer patients (p < 0.05). A negative correlation was found between MT expression and atrophic change (r2 = 0.356, p < 0.01). MT expression in H. pylori positive subjects was gradually recovered after eradication, and increased to the same degree in H. pylori negative ones after two years. Conclusions: H. pylori infection was associated with the enhancement of MT expression in the gastric mucosa, which may indicate that MT expression plays a negative role in the initiation of gastric carcinogenesis. H. pylori eradication may reduce the risk of gastric cancer by leading the increase of MT expression.

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