Preventive effects of chrysin on the development of azoxymethane-induced colonic aberrant crypt foci in rats.
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AbstractThe modifying effects of dietary feeding with chrysin (5,7-dihydroxyflavone) on the development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) were investigated in male F344 rats. We also assessed the effect of chrysin on mitosis and apoptosis in 'normal appearing' crypts. To induce ACF, rats were given two weekly subcutaneous injections of AOM (20 mg/kg body weight). They also received an experimental diet containing chrysin (0.001 or 0.01%) for 4 weeks, starting 1 week before the first dose of AOM. AOM exposure produced a substantial number of ACF (73+/-13/rat) at the end of the study (week 4). Dietary administration of chrysin caused significant reduction in the frequency of ACF: 0.001% chrysin, 37+/-17/rat (49% reduction, P<0.001); and 0.01% chrysin, 40+/-10/rat (45% reduction, P<0.001). In addition, chrysin administration significantly reduced the mitotic index and significantly increased the apoptotic index in 'normal appearing' crypts. These findings might suggest a possible chemopreventive activity of chrysin in the early step of colon tumorigenesis through modulation of cryptal cell proliferation activity and apoptosis.
CitationOncol. Rep. 2006, 15 (5):1169-1173
DescriptionDietary modulation of cancer & cancer biomarkers Dietary item or component studied: chrysinOutcome studied (cancer or cancer biomarker): AOM-induced Aberrant Crypt FociStudy type (in vitro, animals, humans): 32 male F344 rats (group 1: ΑΟΜ alone, group 2: AOM+0.001% chrysin, group3: AOM+0.01 chrysin, group4: 0.01% chrysin, group5: no treatment)Tissue/biological material/sample size: 28-57 crypts/colonMode of exposure (if in vivo): acuteImpact on outcome (including dose-response): 49% reduction by 0.001%chrysin, p<0.001, 45% reduction by 0.01%chrysin, p<0.001Dietary modulation of carcinogenesis-related pathwaysDietary item or component studied: chrysinPathways studied: inhibit the growth by down regulating the expression of PCNA; induce apoptosis via caspase activation and Akt inactivation and cause cell-cycle arrest Study type (in vitro, animals, humans): 32 male F344 rats (group 1: ΑΟΜ alone, group 2: AOM+0.001% chrysin, group3: AOM+0.01 chrysin, group4: 0.01% chrysin, group5: no treatment)Tissue/biological material/sample size: 28-57 crypts/colonMode of exposure (if in vivo) (acute, chronic, root of exposure): acuteImpact on pathway (including dose-response): 26% reduction of mitotic index by 0.001%chrysin and 67% reduction by 0.01%chrysin, p<0.001. Feeding with 0.01%chrysin alone did not affect the mitotic index in the crypts.The apoptotic index or groups 1, 4, 5 were 1.2, 1.2, 0.8 respectively but the values in groups 2, 3 were 3.2, 3.7 respectively, p<0.001. Keywords classification: administration & dosage;Administration,Oral;Agriculture;Animals;Apoptosis;Azoxymethane;Biotechnology;chemically induced;Carcinogens;Chemoprevention;Colonic Neoplasms;drug effects;Diet;dietary modulation of cancer & cancer biomarkers;dietary modulation of carcinogenesis-related pathways;Flavonoids;Food;Injections,Subcutaneous;Japan;Male;Mitosis;prevention & control;Precancerous Conditions;Rats;Rats,Inbred F344;Research;therapeutic use;toxicity;humans;
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