Role of oxygen-derived free radicals in Helicobacter pylori water extract-induced mouse skin carcinogenesis

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...

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Bibliographic Details
Published in:BioFactors (Oxford) 2006, Vol.28 (1), p.1-7
Main Authors: Ishikawa, Takeshi, Yoshida, Norimasa, Tokuda, Harukuni, Kokura, Satoshi, Nakabe, Nami, Kuchide, Masashi, Ichiishi, Eiichiro, Imaeda, Atsumune, Ichikawa, Hiroshi, Naito, Yuji, Okanoue, Takeshi, Yoshikawa, Toshikazu
Format: Article
Language:English
Subjects:
Animals
Antioxidants - pharmacology
Ascorbic Acid - pharmacology
carcinogenesis
Cell Fractionation
Female
H. pylori
Helicobacter pylori
Mice
Mice, Inbred SENCAR
mouse skin carcinogenesis
Mutation
reactive oxygen species
Reactive Oxygen Species - metabolism
Skin Neoplasms - metabolism
Skin Neoplasms - microbiology
Superoxide Dismutase - pharmacology
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Summary: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.
ISSN:0951-6433
1872-8081
DOI:10.1002/biof.5520280101