Affiliations: Department of Gastroenterology, Matsushita Memorial
Hospital, Moriguchi, Japan | Inflammation and Immunology, Graduate School of
Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan | Molecular Gastroenterology and Hepatology, Graduate
School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto,
Japan | Biochemistry, Graduate School of Medical Science,
Kyoto Prefectural University of Medicine, Kyoto, Japan | Safety Research Laboratory, Tanabe Seiyaku Co., Ltd.,
Osaka, Japan
Note: [] Address for correspondence: Norimasa Yoshida, Molecular
Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine,
Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan. Tel.: +81 75 251 5519;
Fax: +81 251 0710; E-mail: nyoshida@koto.kpu-m.ac.jp
Abstract: Helicobacter pylori (H. pylori) infection, the main cause of
chronic gastritis, increases gastric cancer risk. The infection causes
inflammatory cells to produce reactive oxygen metabolites that may damage DNA
and promote carcinogenesis. However, its precise role in gastric carcinogenesis
is as yet unknown. Recently we reported that H. pylori water extract
(HPE) has an initiating activity on two-stage mouse skin carcinogenesis. In
this study, we investigated the effects of anti-oxidants, ascorbic acid and a
combination of superoxide dismutase (CuZnSOD)and catalase, on two-stage mouse
skin carcinogenesis. Ascorbic acid and CuZnSOD/catalase were given to mice
during the period of HPE-initiation. Both the ascorbic acid and
CuZnSOD/catalase treatment attenuated the incidence of tumor formation. The
present results suggest that HPE induces tumor formation via reactive oxygen
species (ROS) production.
Keywords: H. pylori, carcinogenesis, reactive oxygen species, mouse skin carcinogenesis
Journal: BioFactors, vol. 28, no. 1, pp. 1-7, 2006
