above, few trials for prevention, especially in phytochemicals, has been yet to be reported. In this study,
development of edema, erosions, ulcers, and hemorrhage spots in the gastric mucosa were observed after
infection for several months (Table 2), but the mechanism and causal factor contributing to aggravation of
gastric injury induced by physiological stress in a presence of H. pylori remain unknown. We suggested
that oxidative stress was responsible for H. pylori and stress-associated gastric injury, since treatment by an
antioxidant potently prevented H. pylori and stressinduced oxidative DNA damage.