title: Effects of green tea catechins in a rat multi-organ carcinogenesis model.
abstract: The effects of dietary administration of green tea catechins (GTC) were examined using a multi-organ carcinogenesis model. Groups of 15 F344 male rats were initially treated with a single i.p. administration of 100 mg/kg body wt N-diethyl-nitrosamine, 4 i.p. administrations of 20 mg/kg body wt N-methylnitrosourea, 4 s.c. doses of 40 mg/kg body wt 1,2-dimethylhydrazine, together with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine for 2 weeks and then 0.1% 2,2'-dihydroxy-di-n-propylnitrosamine for 2 weeks, both in the drinking water, for a total initiation period of 4 weeks. GTC in the diet, at doses of 1.0 or 0.1%, was administered from 1 day before and during carcinogen exposure, after carcinogen exposure or both during and after carcinogen exposure. Further groups of animals were treated with carcinogen, 1% GTC or basal diet alone as controls. All animals were killed at the end of week 36, and all major organs examined histopathologically. The numbers of small intestinal tumors (adenomas and carcinomas) per rat were significantly reduced in the groups treated with 1% GTC during (0.13 +/- 0.35) and after carcinogen exposure (0.31 +/- 0.48) and in those receiving 1% and 0.1% GTC both during and after carcinogen exposure (0.14 +/- 0.36, 0.46 +/- 0.97 respectively) as compared with the carcinogen alone group (1.07 +/- 1.21). On the other hand, numbers of glutathione S-transferase placental form positive liver foci per cm2 were slightly but significantly increased in the groups treated with 1 and 0.1% GTC during carcinogen exposure, 1% GTC after carcinogen exposure and 1% GTC both during and after carcinogen exposure. The results indicated that while GTC inhibits small intestinal carcinogenesis it slightly enhances hepatocarcinogenesis in a dose dependent manner when applied both during and after carcinogen exposure.
authors.affiliation: First Department of Pathology, Nagoya City University Medical School, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Hirose
authors.forename: T
authors.initials: T
authors.lastname: Hoshiya
authors.forename: K
authors.initials: K
authors.lastname: Akagi
authors.forename: S
authors.initials: S
authors.lastname: Takahashi
authors.forename: Y
authors.initials: Y
authors.lastname: Hara
authors.forename: N
authors.initials: N
authors.lastname: Ito
mesh_terms: D019813:1,2-Dimethylhydrazine; D000236:Adenoma / Q000139:chemically induced / Q000517:prevention & control; D000818:Animals; D016588:Anticarcinogenic Agents / Q000627:therapeutic use*; D001835:Body Weight / Q000187:drug effects; D002085:Butylhydroxybutylnitrosamine; D015197:Carcinogenicity Tests; D002392:Catechin / Q000627:therapeutic use* / Q000633:toxicity; D003043:Cocarcinogenesis; D003110:Colonic Neoplasms / Q000139:chemically induced / Q000517:prevention & control; D004127:Dimethylhydrazines; D004195:Disease Models, Animal; D007414:Intestinal Neoplasms / Q000139:chemically induced / Q000517:prevention & control; D007421:Intestine, Small / Q000187:drug effects; D007680:Kidney Neoplasms / Q000139:chemically induced / Q000517:prevention & control; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced / Q000517:prevention & control; D008175:Lung Neoplasms / Q000139:chemically induced / Q000517:prevention & control; D008297:Male; D008954:Models, Biological; D009374:Neoplasms, Experimental / Q000139:chemically induced / Q000517:prevention & control*; D051381:Rats; D011916:Rats, Inbred F344
chemical_list: D016588:Anticarcinogenic Agents; D004127:Dimethylhydrazines; D002085:Butylhydroxybutylnitrosamine; D002392:Catechin; D019813:1,2-Dimethylhydrazine