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Results for “Azoxymethane”

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At least 451 records · Page 25Linked to original sources
PubMed2006

Flax seed oil and flax seed meal reduce the formation of aberrant crypt foci (ACF) in azoxymethane-induced colon cancer in Fisher 344 male rats.

Flax seed oil and flax seed meal are good sources of omega-3 fatty acids. The objective of this study was to explicate the effects of feeding flax seed oil and flax seed meal on AOM-induced aberrant crypt foci (ACF) in Fisher 344 male rats. Following an acclimatization period, rats were divided into six groups and fed AIN 93G diet Control (C), C+7 and 14% soybean oil (SBO), C+7 and 14% flax seed oil (FSO) and C+10 and 20% flax seed meal (FSM). All rats received 16 mg/kg body weight of AOM at 7 and 8 weeks of age. The rats were euthanized with CO2 at 17 weeks of age. FSM and FSO reduced the incidence of ACF which are putative precursor lesions in the development of colon cancer in the distal colon by 88% and 77%, in the proximal colon by 86% and 87% with a total reduction of 87.5% and 84%, respectively. Glutathione-S-transferase (GST) activities were significantly (P<0.05) higher in rats fed C+7 and 14% FSO and C+10 and 20% FSM, as compared to rats fed C+SBO diets. Results of this study showed that FSO and FSM reduced the incidence of AOM-induced ACF formation and may therefore be effective chemopreventive agents.

Animals↗
PubMed2005

Suppression of azoxymethane-induced colon cancer development in rats by a prostaglandin E receptor EP1-selective antagonist.

Prostaglandin E(2) is involved in colon carcinogenesis through its binding to the PGE(2) receptor subtypes EP(1), EP(2), EP(3) and EP(4). We have demonstrated that administration of ONO-8711, an EP(1)-selective antagonist, suppresses development of AOM-induced ACF in C57BL/6 mice and F344 rats. ONO-8711 also reduced the numbers of intestinal polyps in Min mice. In the present study, we investigated the long-term effects of ONO-8711 on colon cancer development in rats treated with AOM. Male F344 rats were injected subcutaneously with AOM (15 mg/kg body weight) once a week for the first 2 weeks to develop colon cancer. Administration of 400 or 800 p.p.m. ONO-8711 in their diets for 32 weeks reduced the incidence, multiplicity and volume of colon carcinomas. The incidence of colon adenocarcinomas in AOM-treated rats was 97, 83 and 76% (P < 0.05) in the 0, 400 and 800 p.p.m. of ONO-8711 groups, respectively. The multiplicity of adenocarcinomas was also decreased significantly, being 3.31 +/- 0.33, 2.34 +/- 0.27 (P < 0.05) and 2.06 +/- 0.34 (P < 0.01) with 0, 400 and 800 p.p.m. of ONO-8711, respectively. Moreover, treatment with 800 p.p.m. ONO-8711 reduced the mean volume of adenocarcinomas to 49% (P < 0.05) of the value for the AOM treatment alone. Furthermore, the BrdU labeling index was decreased significantly in colon cancer cells by 800 p.p.m. ONO-8711. These results confirm that EP(1) is involved in colon carcinogenesis and that EP(1)-selective antagonists might be promising candidates for colon cancer chemopreventive agents.

Animals↗
PubMed1994

Histochemical studies of progressive p53 mutations during colonic carcinogenesis in Sprague-Dawley rats induced by N-methyl-N-nitro-nitrosoguanidine or azoxymethane.

We studied the increasing expression of the p53 tumor suppressor gene in Sprague-Dawley rats, chemically induced to develop colon cancer. p53 expression was evaluated histochemically at various stages of tumor progression (during a period of 40 weeks) that can be followed by colonic hyperproliferation labeled by 3H-thymidine incorporation. We found that high level nuclear expression of p53 protein correlates with progression of malignancy in carcinogen-induced animals, whereas cytoplasmic staining is related to the onset and early development of malignancy.

Adenocarcinoma↗
PubMed1990

Colonic aberrant crypts in azoxymethane-treated F344 rats have decreased hexosaminidase activity.

Aberrant crypts, identified with methylene blue staining of unsectioned colon from carcinogen-treated rats on the basis of their increased size, were examined for the altered expression of hexosaminidase activity. Previously we identified enzyme-altered foci with normal morphology in sections of colon from carcinogen-treated rats. A reduction of histochemically demonstrable hexosaminidase activity was the most consistent marker for these foci. Aberrant crypts, marked with permanent ink and embedded in methacrylate, had a marked decrease of hexosaminidase activity compared to the adjacent, normal crypts. Hexosaminidase may be a marker that will aid in the identification of the molecular basis of colon cancer in a manner similar to that of esterase D and retinoblastoma.

Animals↗
PubMed1989

[Effects of indomethacin and prostaglandin E2 administered intrarectally on colon carcinogenesis induced by azoxymethane (AOM) in rats].

AOM was administered subcutaneously once a week for 11 consecutive weeks to the rat. On the 15th and 30th week after starting of AOM injection, PGE2 content of the colonic mucosa, tumor and blood of portal vein and NK activity of the spleen and mesenteric lymph node (MLN) were evaluated. On the 15th week, a significant high value of the PGE2 content of colonic mucosa was shown when compared with that of the AOM non-administered group (control group). However, no significant difference was observed in the PGE2 content of blood of portal vein and NK activity of the spleen and MLN. On the 30th week, significant high values of the PGE2 content of AOM-induced tumor and blood of portal vein and low values of NK activity of the spleen and MLN were shown when compared with that of the control group. When indomethacin (IND) was administered intrarectally twice a week for 19 consecutive weeks after completion of AOM injection, induced-colon tumors was significantly suppressed. For this reason, it is important to administer IND at the point when the PGE2 content of colonic mucosa begins to augment.

Administration, Rectal↗
PubMedDate not supplied

Effect of potato starch, cornstarch and sucrose on aberrant crypt foci in rats exposed to azoxymethane.

Studies have shown that different kinds of carbohydrates are able to modify the development of colo-rectal cancer in animals as well as humans. In the present study with rats sucrose and two types of starches were investigated for their effects on the development of aberrant crypt foci (ACF), which have been proposed to represent preneoplastic lesions of colorectal cancer. Fifty-six three-week-old male Wistar rats were randomly assigned to four groups and dosed subcutaneously with AOM (15 mg/kg body wt) once a week for 2 weeks. At the end of the dosing period the animals were allocated to their respective diets. Group I was fed the basic diet; in Group II the carbohydrate pool in the diet was replaced by sucrose, in Group III by potato starch and in Group IV by cornstarch. Animals receiving the potato starch diet showed a statistically significant reduction in body weight gain. A statistically significantly lower number of ACF in all categories but small were demonstrated in animals given potato starch, and in addition an effect was seen in the relative distribution of ACF with fewer of the larger ACF. No effect of sucrose or cornstarch was seen. Explanations of the inhibitory effect in the potato starch group on the development of ACF could either be the lower daily caloric intake or the substantial amounts of resistant starch in the potato starch used.

Animals↗