Chemoprevention of aflatoxin B-1-initiated and carbon tetrachloride-promoted hepatocarcinogenesis in the rat by green tea

Citation
Gz. Qin et al., Chemoprevention of aflatoxin B-1-initiated and carbon tetrachloride-promoted hepatocarcinogenesis in the rat by green tea, NUTR CANCER, 38(2), 2000, pp. 215-222
Citations number
77
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
ISSN journal
01635581 → ACNP
Volume
38
Issue
2
Year of publication
2000
Pages
215 - 222
Database
ISI
SICI code
0163-5581(2000)38:2<215:COABAC>2.0.ZU;2-K
Abstract
Chemoprevention of hepatocarcinogenesis by green tea (GT) has been examined in young male Fischer rats fed AIN-76A diet with aflatoxin B-I (AFB(I)) an d CCl4 as the initiator and promoter, respectively. Animals were administer ed AFB(I) (0.25 mg/kg body wt ip) twice a week for 2 weeks, and 2 weeks lat er, CCl4 was injected (0.8 ml/kg body wt fp) once per week for 11 weeks. Ra ts given 0.5% GT in their drinking water before and during initiation (0-4 wk) or during promotion (6-16 wk) or throughout the experimental period wer e sacrificed 24 hours after the last dose of CCl4, Bromodeoxyuridine incorp oration as a measure of cell proliferation and glutathione S-transferase pl acental form- and gamma -glutamyl transpeptidase positive hepatic foci were analyzed by histochemical methods. Feeding of GT during initiation or prom otion inhibited the number of glutathione S-transferase placental form- and gamma -glutamyl transpeptidase-positive hepatic foci by 30-40% and the are a and volume by 50%. GT treatment throughout the period inhibited the numbe r of both types of hepatic foci by 60% and the area and volume by 75-80%. C ell proliferation was inhibited 35% by GT given during promotion, whereas i nhibition was 65% when GT was given during initiation or throughout the per iod. These results indicate that GT feeding inhibits initiation and promoti on steps of AFB(I) hepatocarcinogenesis and that the inhibition of cell pro liferation is responsible for the inhibition of promotion.