BACKGROUND/AIMS: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors. METHODS: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels. RESULTS: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA. CONCLUSIONS: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.
BACKGROUND/AIMS: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors. METHODS: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels. RESULTS: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA. CONCLUSIONS: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.