Hirose M, Hoshiya T, Akagi K, Takahashi S, Hara Y, Ito N
First Department of Pathology, Nagoya City University Medical School, Japan.
Carcinogenesis. 1993 Aug;14(8):1549-53. doi: 10.1093/carcin/14.8.1549.
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.
使用多器官致癌模型研究了膳食给予绿茶儿茶素（GTC）的效果。将15只F344雄性大鼠分为几组，首先腹腔注射100mg/kg体重的N-二乙基亚硝胺，腹腔注射4次20mg/kg体重的N-甲基亚硝脲，皮下注射4次40mg/kg体重的1,2-二甲基肼，并在饮用水中加入0.05%的N-丁基-N-（4-羟基丁基）亚硝胺，持续2周，然后加入0.1%的2,2'-二羟基二正丙基亚硝胺，持续2周，总启动期为4周。在致癌物暴露前1天及暴露期间、暴露后或暴露期间和暴露后均给予膳食中剂量为1.0%或0.1%的GTC。另外几组动物分别用致癌物、1%GTC或基础饲料单独处理作为对照。在第36周结束时处死所有动物，并对所有主要器官进行组织病理学检查。与单独使用致癌物组（1.07±1.21）相比，在致癌物暴露期间（0.13±0.35）和暴露后接受1%GTC处理的组（0.31±0.48）以及在致癌物暴露期间和暴露后均接受1%和0.1%GTC处理的组（分别为0.14±0.36、0.46±0.97），每只大鼠小肠肿瘤（腺瘤和癌）的数量显著减少。另一方面，在致癌物暴露期间接受1%和0.1%GTC处理的组、暴露后接受1%GTC处理的组以及暴露期间和暴露后均接受1%GTC处理的组，每平方厘米谷胱甘肽S-转移酶胎盘型阳性肝灶的数量略有但显著增加。结果表明，GTC虽然能抑制小肠致癌作用，但在致癌物暴露期间和暴露后应用时，会以剂量依赖的方式轻微增强肝癌发生。
