It is widely reported that reactive oxygen species (ROS) cause apotosis and carcinogenesis. Marked infiltration ofactivated leukocyte and enhanced production of ROS appear to occur in the gastric mucosa infected with Helicobacterpylori (H. pylori). The previous studies reported that the mutation of the succinate dehydrogenase subunit C (SDHC)gene caused the increase in superoxide anion (O2-) and oxidative stress. To extend these findings, we epidemiologicallyinvestigated the association of a SDHC polymorphism at 3’-untranslated region of exon 6 (JST173800) with H. pyloriinfection, gastric atrophy and gastric cancer risk in Japan. The subjects consisted of 454 health checkup examineeswithout a history of cancer and 202 gastric cancer patients. The SDHC polymorphism was not associated with H.pylori infection seropositivity, gastric atrophy, and cancer risk in this study. Although the polymorphism at the 3’-untranslated region could be hypothesized to be functional, this study did not demonstrate any significant associationof the SDHC gene polymorphism with gastric atrophy and cancer.