Nanocurcumin
Amritpal Singh Saroya in Reverse Pharmacology, 2018
A study investigated the effects of polymeric nanocarrier-curcumin on colon cancer in an azoxymethane-induced rat tumor. Forty rats were divided into control, curcumin and polymeric nanocarrier-curcumin-treated groups. Animals received azoxymethane (Fig. 34) as a carcinogenic agent (15 mg/kg, s.c.) weekly for two consecutive weeks. They were given curcumin 0.2% and polymeric nanocarrier-curcumin two weeks before till 14 weeks after the last injection of azoxymethane.
Experimental Colon Carcinogens and Their Mode of Action
Herman Autrup, Gary M. Williams in Experimental Colon Carcinogenesis, 2019
A single s.c. dose of azoxymethane can induce colon cancer.64,109 The compound is somewhat more toxic in mice than in rats. As may be expected, the lower the single dose the longer the latent period in cancer development. Guinea pigs fail to develop colon cancer after AOM administration, but instead exhibit liver cancer, especially endothelial neoplasms.111
Folate/Vitamin B12 Supplementation Combats Oxidative Stress-Associated Carcinogenesis in a Rat Model of Colon Cancer
Published in Nutrition and Cancer, 2019
Smitha Padmanabhan, Mostafa I. Waly, Varna Taranikanti, Nejib Guizani, Amanat Ali, Mohammad S. Rahman, Zaher Al-Attabi, Raya N. Al-Malky, Sultan N. M. Al-Maskari, Bader R. S. Al-Ruqaishi, Jianan Dong, Richard C. Deth
Animal studies have provided significant insight into the active role of oxidative stress as a trigger for CRC carcinogenesis (12,13). Azoxymethane (AOM) is a potent carcinogenic agent that is commonly used to induce oxidative stress cancer in rat colon (14,15). Several experimental models of CRC suggest that dietary antioxidants and functional foods can prevent early steps of CRC development (i.e., aberrant crypt foci and adenomatous polyp formation); yet, no recent studies have examined the biochemical and histopathological effects of folate and vitamin B12 supplementation in relation to CRC development (12–17). Therefore, this study was undertaken to investigate a potential protective effect of folate and vitamin B12 against AOM-induced colon cancer and oxidative stress in rats, as an experimental model for CRC.
Personalized Nutrition in Disrupting Cancer — Proceedings From the 2017 American College of Nutrition Annual Meeting
Published in Journal of the American College of Nutrition, 2019
Taylor C. Wallace, Scott Bultman, Chris D’Adamo, Carrie R. Daniel, Justine Debelius, Emily Ho, Heather Eliassen, Dawn Lemanne, Purna Mukherjee, Thomas N. Seyfried, Qiang Tian, Linda T. Vahdat
Diets rich in dietary fiber have been associated with lower rates of colorectal cancer (46). This effect has been attributed to two mechanisms: First, fiber is associated with increased transit time, which is hypothesized to decrease colonic exposure to carcinogens. Fiber is also thought to interact with the microbiome to produce tumor-suppressive metabolites. Recent work has implicated butyrate. Using a gnotobiotic mouse model (i.e., a mouse model in which only certain known strains of bacteria and other microorganisms are present), the relationship between SCFA fermenting bacteria, dietary fiber, and colorectal cancer was evaluated. Gnotobiotic mice allow direct perturbations of the microbiota while controlling for potentially confounding effects such as genetic background or food source. To evaluate the interaction between the microbiome and fiber in regulating colorectal cancer, gnotobiotic mice were inoculated with a consortium of four commensal bacteria with or without Butyrivibrio fibrisiolvens, a butyrate producer. Mice were fed high- or low-fiber chow. Colorectal cancer was then induced using the azoxymethane model. Tumor attenuation was seen only in mice that received both B. fibrisiolvens and dietary fiber, suggesting that fermentation to butyrate was required for the tumor-suppressive effect. The suppression could also be induced using a butyrate-fortified diet, supporting the role of microbial fermentation of dietary fiber in colorectal cancer prevention (47).
Methanolic Extract of Muntingia Calabura L. Mitigates 1,2-Dimethyl Hydrazine Induced Colon Carcinogenesis in Wistar Rats
Published in Nutrition and Cancer, 2021
Ninan Jisha, A. Vysakh, V. Vijeesh, P. S. Anand, M. S. Latha
1,2-Dimethyl hydrazine (DMH) is a colon specific carcinogen widely used in experimental animals to induce colorectal tumors (5). DMH induced CRC emanates from various molecular and histopathological alterations in the colonic epithelium like the development of aberrant crypt foci (ACF) and mucin depleted foci (MDF) (6). ACF and MDF are the preneoplastic leisions that may contribute to the progression of colonic epithelial transformation into colorectal carcinoma which are considered as the early biomarkers of CRC (7, 8). The DMH is metabolized initially in the liver and transported to colon as glucoronide conjugates via bile or blood (9, 10) and further degraded into azomethane. The azoxymethane generated from azomethane by the process of oxidation (N-oxidation) undergoes hydroxylation to form methylazoxymethanol (an unstable compound) which readily generates a highly reactive electrophilic methyl diazonium ion. This process causes the release of methyl free radicals meanwhile in the presence of metal ions, DMH causes the generation of hydroxyl radical or hydrogen peroxide which evokes oxidative stress as a result of the imbalance between the ROS and endogenous antioxidants (11, 12). Oxidative stress further progresses to inflammation which finally promotes CRC.
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