INTRODUCTION: Helicobacter pylori infection has been shown to cause inflammation, increased production of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. However, the effect of eradication treatment on DNA damage in patients infected with H. pylori is unclear. OBJECTIVES: The objective of this study was to investigate the effect of eradication treatment on peripheral DNA damage and oxidative status in patients wth H. pylori infection. PATIENTS AND METHODS: The study involved 42 patients positive for H. pylori (Hp+) and 25 patients negative for H. pylori (Hp-). Peripheral lymphocyte DNA damage was assessed using the alkaline comet assay and plasma oxidative status was determined. Measurements were conducted at baseline and 2 weeks after eradication treatment. RESULTS: The total antioxidant status (TAS) was lower in Hp+ patients than in Hp- patients (P <0.05), while the total oxidant status (TOS), oxidative stress index (OSI), and peripheral lymphocyte DNA damage were higher (P <0.001 for all parameters). TOS, OSI, and peripheral lymphocyte DNA damage were significantly lower after eradication treatment (P <0.001 for all parameters), while TAS was significantly higher (P <0.05). There was no correlation between TOS, OSI, peripheral lymphocyte DNA damage, and TAS and the histopathological degree of antral gastric inflammation in the Hp+ group (P >0.05). CONCLUSIONS: Our results suggest that H. pylori eradication significantly decreases peripheral lymphocyte DNA damage and oxidative stress. Eradication treatment might help prevent the development of gastric cancer in patients with H. pylori infection.
INTRODUCTION:Helicobacter pyloriinfection has been shown to cause inflammation, increased production of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. However, the effect of eradication treatment on DNA damage in patients infected with H. pylori is unclear. OBJECTIVES: The objective of this study was to investigate the effect of eradication treatment on peripheral DNA damage and oxidative status in patients wth H. pyloriinfection. PATIENTS AND METHODS: The study involved 42 patients positive for H. pylori (Hp+) and 25 patients negative for H. pylori (Hp-). Peripheral lymphocyte DNA damage was assessed using the alkaline comet assay and plasma oxidative status was determined. Measurements were conducted at baseline and 2 weeks after eradication treatment. RESULTS: The total antioxidant status (TAS) was lower in Hp+ patients than in Hp- patients (P <0.05), while the total oxidant status (TOS), oxidative stress index (OSI), and peripheral lymphocyte DNA damage were higher (P <0.001 for all parameters). TOS, OSI, and peripheral lymphocyte DNA damage were significantly lower after eradication treatment (P <0.001 for all parameters), while TAS was significantly higher (P <0.05). There was no correlation between TOS, OSI, peripheral lymphocyte DNA damage, and TAS and the histopathological degree of antral gastric inflammation in the Hp+ group (P >0.05). CONCLUSIONS: Our results suggest that H. pylori eradication significantly decreases peripheral lymphocyte DNA damage and oxidative stress. Eradication treatment might help prevent the development of gastric cancer in patients with H. pyloriinfection.