• Journal of Nutrition and Health
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• v.32 no.4
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• pp.394-400
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• 1999

Since it has generally been considered that high-hat diets promote carcinogenesis, fat intake of less than 30% of total calories has been recommended to reduce the risk of cancer. Specific dietary guidelines for fat intake to reduce the risk of colon cancer have not yet been established. In order to determine the level of dietary fat needed the risk of colon cancer, rats were fed one of four experimental fat diets, very low(7% of total calories from corn oil, VLC), low(15% LC), medium (30%, MC), and high fat(45%, HC). Cell proliferation as an intermediate biomarker of color carcinogenesis was measured by the in vivo incorporation of bromodeoxyuridine into DNA. Fecal lipid excretion was measured by gravimetric method. As fat levels in the diet increased, fecal lipid concentrations also increased (VLC

• Nutritional Sciences
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• v.2 no.2
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• pp.71-75
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• 1999

Epidemiologic studies consistently demonstrate an inverse relationship between risk for colon canter and consumption of fruits and vegetables. Wheat bran, flax and soy contain dietary fiber and phytochemicals, such as lignans and isoflavones, that may inhibit colon carcinogenesis. Orange juice contains hesperidin, a flavanone glucoside that protects against colon carcinogenesis. This study determined if feeding orange juice, wheat bran, soy and flaxseed (combined diet) would inhibit azoxymethane (AOM) induced colon cancer. Cancer was initiated in male Fisher 344 rats by injecting 15 mg AOM/kg of weight at 22 and 29 days of age. One week after the second AOM injection, rats (N = 30) in the combined diet group received dry diet containing wheat bran (4%), soy with ethanol soluble phytochemirals(13%) and flaxseed (8%) and orange juice replaced drinking water. The control group remained on the control diet and received distilled water to drink. The rats were killed 28 weeks later, and colon tissues and tumors were removed for histologic analysis. Feeding the combined diet significantly reduced tumor incidence (p < 0.05), however tumor multiplicity was not changed (p > 0.05, 0.9 tumors/rat fed the combined diet vs 1.2 for controls). Also, tumor burden was only marginally reduced in rats fed the combined diet vs control rats (65 vs 210 mg of tumor/rats, respectively). The reduction in tumor incidence was associated with a decreased labeling index and proliferation zone in normal appearing colon mucosa. Therefore, this study shows that phytochemicals in wheat bran, soy, flax and orange juice reduce colon carcinogenesis, presumably by decreasing cell proliferation and enhancing cell differentiation.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1569-1573
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• 2012

Luteolin (LUT), a bioflavonoid has been used as a chemopreventive agent world-wide against chemically induced cancer. Hence we designed an experiment to assess chemopreventive action of LUT on lipid peroxidation (LPO) and glycoconjugates in azoxymethane (AOM)-induced colon carcinogenesis. Colon cancer was induced by 15 mg/body kg. body weight of AOM and administration of LUT (at the dose of 1.2 mg/kg. body weight) was till end of the study. Analysis of lipid peroxidative end products such as protein carbonyl (PC), malonadehyde (MDA) and conjucated dienes (CD) demonstrated significant increase in in AOM-induced animals with reduction by LUT (p<0.05). Increased levels of glycoconjugates such as hexose, hexosamine, sialic acid, fucose and mucoprotein were analyzed in serum and colon tissues examined histopathologically by periodic acid Schiff's (PAS) staining were also reversed by LUT l(p<0.05). The secondary marker of colon cancer mucin depleted foci (MDF) was assessed in control and experimental group of animals. A characteristic increase of MDF was observed in AOM-induced colon cancer animals. Treatment with LUT decreased the incidence of MDF. These results suggest that LUT alters the expression of glycoconjugates and suppress colon cancer. Hence, we speculate that LUT can be used as a chemopreventive agent to treat colon cancer.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.91-91
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• 2003

Colon cancer is one of the most common malignancies in humans, and the search for effective chemopreventive agents is an important and urgent task. Expression levels of inflammation-related enzymes, cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) are elevated in colon cancers, and their products, prostaglandins and nitric oxide, are suggested to be involved in colon carcinogenesis.(omitted)

• Preventive Nutrition and Food Science
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• v.22 no.2
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• pp.149-155
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• 2017

The effects of Korean solar salt on an azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced colon cancer C57BL/6 mouse model were studied. Korean solar salt samples (SS-S, solar salt from S salt field; SS-Yb, solar salt from Yb salt field), nine-time-baked bamboo salt (BS-9x, made from SS-Yb), purified salt (PS), and SS-G (solar salt from $Gu\acute{e}rande$, France) were orally administered at a concentration of 1% during AOM/DSS colon cancer induction, and compared for their protective effects during colon carcinogenesis in C57BL/6 mice. SS-S and SS-Yb suppressed colon length shortening and tumor counts in mouse colons. Histological evaluation by hematoxylin and eosin staining also revealed suppression of tumorigenesis by SS-S. Conversely, PS and SS-G did not show a similar suppressive efficacy as Korean solar salt. SS-S and SS-Yb promoted colon mRNA expression of an apoptosis-related factor and cell-cycle-related gene and suppressed pro-inflammatory factor. SS-Yb baked into BS-9x further promoted these anti-carcinogenic efficacies. Taken together, the results indicate that Korean solar salt, especially SS-S and SS-Yb, exhibited anti-cancer activity by modulating apoptosis- and inflammation-related gene expression during colon carcinogenesis in mice, and bamboo salt baked from SS-Yb showed enhanced anti-cancer functionality.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.1
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• pp.73-80
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• 2016

Colorectal cancer is a very prevalent diagnosed cancer. The current study was performed in order to examine the role of BRAE (Basella rubra aqueous extract) in regulating aberrant crypt foci (ACF) formation, cell proliferation and inhibition of apoptosis in a colon carcinogenesis model in male Wistar rats. Rats were randomly allocated into six groups. Group I served as control, and group II acted as a drug control administered BRAE (250mg/kg b.w.) orally for 30 weeks. Rats in group III-VI were given subcutaneous injections of DMH (25mg/kg b.w. weekly) for 15 weeks to initiate colon carcinogenesis. Those in group IV and VI were administered BRAE along with DMH injections. Rats in group V were administered with BRAE after cessation of DMH injection. After 30 weeks of experimental period colons were obtained from experimental groups and analyzed for ACF incidence, argyrophilic nucleolar organizing region-associated proteins (AgNOR) count, histopathological and immunohistochemical changes. Only in DMH exposed groups were ACF and AgNOR numbers increased. Administration of BRAE appreciably decreased the numbers of ACF and AgNOR in BRAE treated groups. Histopathological findings revealed a high level of dysplastic changes with decreased number of goblet cells found only in only DMH injected rats. Administration of BRAE in treated group rats reversed these changes. Expression markers for cell proliferation (PCNA and Ki67) were elevated in DMH treated rats, but reduced with BRAE treatement. This expression was reversed with apoptosis markers (p53 and Caspase-3). Thus the results results of the present study were found to be significant and confirmed the potential efficacy of BRAE against colon carcinogenesis.

• Korean Journal of Veterinary Pathology
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• v.5 no.1
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• pp.29-34
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• 2001

This study was conducted to assess the chemopreventive effects of chitosan in a rat colon carcinogenesis induced by azoxymethane (AOM). Ninety, 5-week-old, male F344 rats were divided into three groups. The animals in group 1 received subcutaneous injections of 15mg/kg AOM three times for two weeks, then were placed on powdered basal diet containing 2% chitosan for 37 weeks from weeks 3 to 40. The animals in group 2 were given AOM alone. The animals in group 3 were given 2% chitosan without prior carcinogen treatment. All animals were sacrificed at week 12 for quantitative analysis of aberrant crypt foci (ACF) and at week 40 fur analysis of tumor induction. Total numbers of ACF and AC per colon of group 1 were not significantly different from those of group 2. Tumor incidences and multiplicities of small intestine in the group 1 were significantly decreased compared with those of the group 2 (P<0.05). According to pathological diagnoses, adenocarcinoma incidence and multiplicity in the small and large intestine in the group 1 were significantly decreased compared with those of the group 2 (p<0.05). No toxic effects were observed in animals given chitosan in terms of body weights, and liver or kidney histology. These results indicate that chitosan may have a potential as chemopreventive agents of colon carcinogenesis during the postinitiation stage.

• Food Science and Biotechnology
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• v.16 no.6
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• pp.1064-1068
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• 2007

We evaluated the effect of soybean dongchunghacho [SD, cultivated dongchunghacho fungus (Paecilomyces tenuipes) on soybeans] on dimethylhydrazine (DMH)-induced DNA damage and oxidative stress in male F344 rats. The animals were divided into 3 groups and fed a casein-based high-fat, low fiber diet without (DMH group) or with 13%(w/w) of soybean (DMH+S group), or SD (DMH+SD group). One week after beginning the diets, rats were treated weekly with DMH (30 mg/kg, s.c.) for 6 weeks; dietary treatments were continued for the entire experiment and endpoints measured at 9 weeks after the first DMH injection. SD supplementation reduced DMH-induced DNA damage in colon cells and reduced plasma lipid peroxidation. Thus, SD may have therapeutic potential for early-stage colon carcinogenesis.

• Natural Product Sciences
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• v.5 no.1
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• pp.48-53
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• 1999

There are epidemiological evidences that the population with high fecal ${\beta}-glucuronidase$ activity has greater risk of colon cancer than the population with low fecal ${\beta}-glucuronidase$. This relationship was investigated by using the mouse-dimethylhydrazine colon carcinogenesis model and the extract of antler which was a ${\beta}-glucuronidase$ inhibitor. Mice with low fecal ${\beta}-glucuronidase$ activity induced by administration of water and Folch's fraction of antler had significantly fewer aberrant crypts after injections of 1,2-dimethylhydrazine (DMH) than mice treated with DMH alone. The result supports the hypothesis that the inhibitor of ${\beta}-glucuronidase$ such as antler extract can protect an animal against the induction of colon cancer.

• Archives of Pharmacal Research
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• v.18 no.2
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• pp.79-83
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• 1995

There is epidemilogical evidence that the population with high fecal ${\beta}-glucuronidase$activity has greater risk of colon cancer than the population with low facal ${\beta}-glucuronidase$. This relationship was investigated by using the mouse-dimethylhydrazine colon carcinogenesis model and the fraction of Glucidum which is a .${\beta}-glucuronidase$inhibitor. Mice with low facal ${\beta}-glucuronidase$activity induced by consumption of the ether fraction of G lucidum had significantly fewer aberrant crypts(AC) after injections of 1, 2-dimethylhydeazine (DMH) than mice treated with DMH alone. The result supports the hypothesis that the inhibitor such as the ether fraction of G lucidum can protect an animal against the induction of colon cancer.