A comparison of whole wheat, refined wheat and wheat bran as inhibitors of heterocyclic amines in the Salmonella mutagenicity assay and in the rat colonic aberrant crypt focus assay.
Refined wheat, unrefined whole wheat, and wheat bran were studied for their ability to protect against heterocyclic amines (HCAs) in vitro and in vivo. Wheat bran, which binds HCAs in vitro, as well as refined wheat and unrefined whole wheat, inhibited the mutagenic activities of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) when they were co-incubated and the supernatant (minus grain) was added to the Salmonella assay. The water-soluble fraction alone from refined and unrefined wheat, but not bran, also inhibited against these mutagens in vitro. In vivo, AIN-93G diets containing refined wheat or unrefined wheat were examined for their ability to inhibit IQ-induced colonic aberrant crypt foci (ACF) in the Fischer 344 rat. A slight increase in the number of AC/ACF (aberrant crypts/ACF) was seen after 16 weeks in rats treated post-initiation with refined wheat (P < 0.05), and fewer foci with two or three aberrant crypts (ACF-2) were found in rats given unrefined whole wheat post-initiation compared with animals treated with the same diet during the initiation phase (P < 0.05). There was no significant difference in the profile of IQ urinary metabolites or excretion of promutagens 0-48 h after carcinogen dosing, and grains had no effect on hepatic cytochrome P4501A1 (CYP1A1), CYP1A2, aryl sulfotransferase or N-acetyltransferase activities; however, a slightly higher UDP-glucuronosyl transferase activity was observed in rats fed unrefined wheat compared with refined wheat diets (P < 0.05). Thus, despite their antimutagenic activities in vitro, only marginal effects were seen with refined and unrefined wheat in vivo with respect to hepatic enzyme activities, carcinogen metabolism and IQ-induced ACF in the rat colon.
Yu
Z
Z
Linus Pauling Institute, USA.
Xu
M
M
Santana-Rios
G
G
Shen
R
R
Izquierdo-Pulido
M
M
Williams
D E
DE
Dashwood
R H
RH
D000588:Amines / Q000037:antagonists & inhibitors / Q000633:toxicity*; D000818:Animals; D016587:Antimutagenic Agents; D002273:Carcinogens / Q000633:toxicity; D003106:Colon / Q000187:drug effects / Q000473:pathology; D003110:Colonic Neoplasms / Q000139:chemically induced / Q000517:prevention & control; D004043:Dietary Fiber / Q000008:administration & dosage; D006863:Hydrogen-Ion Concentration; D007093:Imidazoles / Q000633:toxicity; D009152:Mutagenicity Tests; D011804:Quinolines / Q000633:toxicity; D051381:Rats; D011916:Rats, Inbred F344; D012475:Salmonella / Q000187:drug effects / Q000235:genetics; D012995:Solubility; D014908:Triticum / Q000737:chemistry
D000588:Amines; D016587:Antimutagenic Agents; D002273:Carcinogens; D004043:Dietary Fiber; D007093:Imidazoles; D011804:Quinolines; C049584:2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine; C036989:2-amino-3,4-dimethylimidazo(4,5-f)quinoline