INHIBITION BY GREEN TEA EXTRACT OF DIETHYLNITROSAMINE-INITIATED BUT NOT CHOLINE-DEFICIENT, L-AMINO ACID-DEFINED DIET-ASSOCIATED DEVELOPMENTOF PUTATIVE PRENEOPLASTIC, GLUTATHIONE-S-TRANSFERASE PLACENTAL FORM-POSITIVE LESIONS IN RAT-LIVER

The effects of green tea extract (GTE) on exogenous and endogenous mod els of rat liver carcinogenesis using diethylnitrosamine (DEN) and a c holine-deficient, L-amino acid-defined (CDAA) diet were studied. For t he exogenous carcinogenesis study, male Fischer 344 rats, 6 weeks old, were given a single intraperitoneal dose of 200 mg/kg body weight of DEN, partially hepatectomized at week 3, and administered GTE at doses of 0, 0.01 and 0.1% in the drinking water from week 2 for 10 weeks. F or the endogenous carcinogenesis study, rats were fed the CDAA diet an d simultaneously given GTE for 12 weeks. All rats were killed at the e nd of week 12. After DEN-initiation, the apparent numbers of glutathio ne S-transferase placental form-positive foci, assayed as putative pre neoplastic lesions, were decreased by the administration of GTE, thoug h their sizes were not altered. In contrast, GTE did not significantly reduce the numbers of the lesions induced by the CDAA diet or affect their sizes. While the levels of 8-hydroxyguanine, a parameter of oxid ative DNA damage, were reduced by the GTE administration in both exper imental models, GTE did not protect against the CDAA-diet-associated l iver tissue damage in terms of either histology or plasma marker enzym e levels. We conclude that, while GTE may be a possible chemopreventiv e agent for nitrosamine-initiated hepatocarcinogenesis in the absence of chronic hepatocyte damage, it does not significantly inhibit lesion development in hepatocarcinogenesis associated with the CDAA diet, a cirrhosis-associated model.