Keiji Wakabayashi
Cancer Prevention Division, National Cancer Center Research Institute
5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
(Tel: 81-3-3547-5271 Fax: 81-3-3543-9305 E-mail: kwakabay@gan2.ncc.go.jp)
Gastric cancer is one of the most common malignancies in the world. A high intake of salted foods and an insufficient consumption of fresh fruits and vegetables are reported to be involved as causal factors of the gastric cancer. In addition, there is a positive relationship between Helicobacter pylori infection and the development of gastric lesions including gastritis, peptic ulcers and gastric cancers (1). It has been suggested that H. pylori-induced gastritis and ulceration are affected by H. pylori strain diversity, as well as host and environmental factors including diet.
Recently, Mongolian gerbils were reported to be readily colonized by H. pylori with associated development of chronic gastritis, gastric ulcers, and intestinal metaplasia after prolonged infection (2). As part of the search for dietary factors influencing H. pylori-induced gastritis, the effects of fish meal in conventional diet were examined in Mongolian gerbils. After inoculation of H. pylori, diet containing 10% fish meal was given to the animals for four weeks. Edematous thickening with severe neutrophil and mononuclear cell infiltration in both the mucosa and submucosa of the glandular stomach was observed in almost all the animals. These gastric lesions were enhanced by a 20% fish meal supplement. However, such gastric lesions were not observed in infected animals fed a fish meal free diet, 10% casein or 10% beef diet, although almost the same numbers of viable H. pylori were detected as in the fish meal diet case. No gastric lesions were detected in the 10% and 20% fish meal groups without H. pylori inoculation (3). Identification of the gastritis-enhancing factors in fish meal is now under investigation.
Many factors including Cag A, Vac A and urease have been proposed to play roles in determining the virulence of H. pylori-associated disease. We recently found that urease inhibitors have a marked ability to suppress H.pylori-induced gastritis and also eradicate colonized H. pylori in Mongolian gerbils. This suggests that urease plays an important role in H. pylori colonization and induction of the gastritis. To identify diets reducing H. pylori-induced gastric lesions, we are now searching for foodstuffs which contain urease inhibitors.
References:
(1) Parsonnet, J., Friedman, G.D., Vandersteen, D.P., Chang, Y., Vogelman, J.H., Orentreich, N. & Sibley, R.K. 1991). Helicobacter pylori infection and the risk of gastric carcinoma. N. Engl. J. Med., 325:1127-1131
(2) Hirayama, F., Takagi, S., Kusuhara, H., Iwao, E., Yokoyama, Y. & Ikeda, Y. (1996). Induction of gastric ulcer and intestinal metaplasia in Mongolian gerbils infected with Helicobacter pylori. J. Gastroenterol., 31:755-757
(3) Tanigawa, T., Kawamori, T., Iimuro, M., Ohta, T., Higuchi, K., Arakawa, T., Sugimura, T. & Wakabayashi, K. (2000). Marked enhancement by fish meal of Helicobacter pylori-induced gastritis in Mongolian gerbils. Jpn. J. Cancer Res., 91:769-773
Keiji Wakabayashi PhD 1971 Shizuoka College of Pharmacy, B. Pharm. Sci.,
1977 Shizuoka College of Pharmacy, Ph.D.
1979 Research Staff, Natl. Cancer Ctr. Res. Inst.
1994- Chief of Biochemistry Div., Natl. Cancer Ctr. Res. Inst.
1995- Chief of Cancer Prevention Div., Natl. Cancer Ctr. Res. Inst.
Speciality and Special Interest:
Food-derived mutagens and carcinogens, and their DNA modification.
Chemoprevention by dietary factors and medicines.