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Effects of quercetin and β‐carotene supplementation on azoxymethane‐induced colon carcinogenesis and inflammatory responses in rats fed with high‐fat diet rich in ω‐6 fatty acids
Author(s) -
Choi SooYeon,
Park Jung Han Yoon,
Kim JongSang,
Kim Mi Kyung,
Aruoma Okezie I.,
Sung MiKyung
Publication year - 2006
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520270112
Subject(s) - azoxymethane , aberrant crypt foci , medicine , endocrinology , crypt , quercetin , inflammation , nitric oxide synthase , nitric oxide , prostaglandin e2 , carotene , carcinogenesis , colorectal cancer , chemistry , cancer , antioxidant , food science , biochemistry , colonic disease
Chronic inflammation in gastrointestinal tract has been suggested as a risk factor for tumor formation. The effect of dietary supplementation of quercetin or ß‐carotene on colon carcinogenesis and inflammatory response in rats fed with high‐fat diet rich in ω‐6 fatty acids was assessed. Animals were exposed to two weekly subcutaneous injections of AOM (azoxymethane) at a single dose of 15 mg/kg body weight. A portion of rats from each group was sacrificed at 8 weeks after the last AOM treatment to determine ACF (aberrant crypt foci) formation. Colonic mucosa expression of iNOS (inducible nitric oxide) and COX‐2 (cyclooxygenase‐2) protein, and blood PGE 2 (prostaglandin E 2 ) level were measured. The remaining groups of animals were sacrificed at 33 weeks after the last AOM treatment to examine colon tumor formation. Rats on high‐fat diet developed more aberrant crypt foci (P<0.05) compared with those of rats on regular diet. In the same vein, but in contrast to the effect seen with regular diet, the high‐fat diet induced a significant up‐regulation of iNOS expression. There was no significant change in the extent of COX‐2 expression or in the PGE 2 levels. Quercetin or β‐carotene supplementation reduced the number of ACF only in animals fed high‐fat diet (p<0.05), however, no significant difference in tumor incidence was found. At week 33, the expression of iNOS was reduced by quercetin without a statistical significance, and COX‐2 expression was slightly reduced in rats on ß‐carotene supplementation. No change in PGE 2 levels was observed. Whilst dietary antioxidants are considered as effective suppressors for precancerous lesion formation in colons exposed to high‐risk diet, it is clear that elucidating the role of individual antioxidants in colon tumor formation coupled with an understanding of the molecular mechanisms involved would benefit colon cancer prevention strategies.