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
K. Tamura et al., 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, Japanese journal of cancer research, 88(4), 1997, pp. 356-362
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.