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Naphthoquinone Constituents of Anticancer Terrestrial Plants
Published in Spyridon E. Kintzios, Maria G. Barberaki, Evangelia A. Flampouri, Plants That Fight Cancer, 2019
In animal experiments, the i.p. administration of 7 (2 mg/kg, five injections per week for 11 weeks), beginning three days after the subcutaneous implantation of hormone-resistant prostate cancer DU145 cells (2.5 × 106 cells), delayed tumor growth by three weeks and reduced both tumor weight and volume by 90% (Aziz et al. 2008). The results of in vivo efficacy evaluations also indicated that plumbagin (1 mg/kg, i.p. for 21 times in 21 days) resulted in a 57% reduction in human ovarian OVCAR-5 xenograft volume (n = 10; 330.0 ± 227.0 mm3) as compared to the solvent alone group (n = 10; 776.8 ± 155.7 mm3) (Sinha et al. 2013). Meanwhile, it was also effective in the pancreatic PANC-1 ectopic xenograft model since treatment of the natural 1,4-naphthoquinone (2mg/kg, i.p. injection for five days a week) showed significant (P < 0.01) inhibition on both tumor growth (50%) and tumor weight (50%), when compared with the control groups (Hafeez et al. 2014). In addition to its antiproliferative activity, plumbagin also exhibited chemopreventive effects against the azoxymethane-induced intestinal carcinogenesis in animals, suggesting its chemopreventive activity (Sugie et al. 1998). It could inhibit both the ultraviolet radiation-induced cutaneous damage and the development of squamous cell carcinomas and was recognized as promising chemopreventive agents for human cancers (Sand et al. 2010).
Experimental Colon Carcinogens and Their Mode of Action
Published in Herman Autrup, Gary M. Williams, Experimental Colon Carcinogenesis, 2019
John H. Weisburger, Emerich S. Fiala
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
Nanocurcumin
Published in Amritpal Singh Saroya, 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.
The Protective Role of Urtica dioica Seed Extract Against Azoxymethane-Induced Colon Carcinogenesis in Rats
Published in Nutrition and Cancer, 2022
Ahmet Uyar, Abdulahad Doğan, Turan Yaman, Ömer Faruk Keleş, Zabit Yener, İsmail Çelik, Elif Ebru Alkan
Azoxymethane (AOM) (C2H6N2O) a potent organotropic colon carcinogen and a metabolite of 1,2-Dimethylhydrazine (DMH), has commonly been used to induce colon neoplasia in rodents (6). On the other hand, it is also used in experimental models of the underlying mechanisms of human sporadic colon cancer in order that formation of this cancer closely mirrors the pattern seen in humans (7). Following AOM treatment, the epithelial cells undergo pathogenesis from minor lesion such as aberrant crypt foci (ACF) to major lesions including adenoma and malignant adenocarcinoma (8). ACFs are presumed pre-cancer lesions that form in the colorectal area of both animal models and humans (9). These foci have been used as intermediate biomarkers to rapidly evaluate the chemopreventive potential of several agents, including naturally occurring agents against colon cancer (10).
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.
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).