title: Inhibition by white tea of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-induced colonic aberrant crypts in the F344 rat.
abstract: There is growing interest in the potential health benefits of tea, including the anticarcinogenic properties. We report here that white tea, the least processed form of tea, is a potent inhibitor of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced colonic aberrant crypts in the rat. Male Fischer 344 rats were treated for 8 wk with white tea (2% wt/vol) or drinking water alone, and on alternating days in experimental Weeks 3 and 4 the animals were given PhIP (150 mg/kg body wt p.o.) or vehicle alone. At the end of the study there were 5.65 +/- 0.81 and 1.31 +/- 0.27 (SD) aberrant crypt foci per colon in groups given PhIP and PhIP + white tea, respectively (n = 12, P < 0.05). No changes were detected in N-acetyltransferase or arylsulfotransferase activities compared with controls, but there was marked induction of ethoxyresorufin O-deethylase, methoxyresorufin O-demethylase, and UDP-glucuronosyltransferase after treatment with white tea. Western blot revealed corresponding increases in cytochrome P-450 1A1 and 1A2 proteins. Enzyme assays and Western blot also revealed induction of glutathione S-transferase by white tea. There was less parent compound and 4'-hydroxy-PhIP but more PhIP-4'-O-glucuronide and PhIP-4'-O-sulfate in the urine from rats given PhIP + white tea than in urine from animals given carcinogen + drinking water. The results indicate that white tea inhibits PhIP-induced aberrant crypt foci by altering the expression of carcinogen-metabolizing enzymes, such that there is increased ring hydroxylation at the 4' position coupled with enhanced phase 2 conjugation.
authors.affiliation: Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA.
authors.forename: G
authors.initials: G
authors.lastname: Santana-Rios
authors.forename: G A
authors.initials: GA
authors.lastname: Orner
authors.forename: M
authors.initials: M
authors.lastname: Xu
authors.forename: M
authors.initials: M
authors.lastname: Izquierdo-Pulido
authors.forename: R H
authors.initials: RH
authors.lastname: Dashwood
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000008:administration & dosage; D003106:Colon / Q000473:pathology*; D003110:Colonic Neoplasms / Q000139:chemically induced / Q000517:prevention & control*; D019363:Cytochrome P-450 CYP1A1 / Q000096:biosynthesis; D019388:Cytochrome P-450 CYP1A2 / Q000096:biosynthesis; D003577:Cytochrome P-450 Enzyme System / Q000096:biosynthesis; D004790:Enzyme Induction; D020719:Glucuronides / Q000652:urine; D014453:Glucuronosyltransferase / Q000096:biosynthesis; D005982:Glutathione Transferase / Q000096:biosynthesis; D007093:Imidazoles / Q000652:urine; D008297:Male; D010088:Oxidoreductases / Q000096:biosynthesis; D011230:Precancerous Conditions / Q000517:prevention & control*; D051381:Rats; D011916:Rats, Inbred F344; D013431:Sulfates / Q000652:urine; D013662:Tea
chemical_list: D016588:Anticarcinogenic Agents; D020719:Glucuronides; D007093:Imidazoles; D013431:Sulfates; D013662:Tea; D003577:Cytochrome P-450 Enzyme System; C049584:2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine; D010088:Oxidoreductases; C076307:methoxyresorufin-O-demethylase; D019363:Cytochrome P-450 CYP1A1; D019388:Cytochrome P-450 CYP1A2; D014453:Glucuronosyltransferase; D005982:Glutathione Transferase