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In Vivo Induction of Colon Cancer Dose and Animal Species
Published in Herman Autrup, Gary M. Williams, Experimental Colon Carcinogenesis, 2019
DMH and its closely related compound, azoxymethane, are two of the most potent and most commonly used carcinogens for experimental colon carcinogenesis. Both of these compounds are chemically related to cycasin.35 Despite the differences in doses, schedules, and animal strains used by different investigators,35–37 there is some consistency in their results in using DMH as the carcinogen for animal models. When DMH is given on a weekly basis and the induction time is sufficient (16 to 24 weeks), approximately 100% of the experimental animals develop tumors. These tumors occur predominantly in the large bowel. The mode of tumor formation in the DMH model seems to be species specific. In rats, the neoplasms are short-stalked, discrete, and distributed in the ascending and descending colon, while in mice they are broad based and occur diffusely in the distal colon and rectum. Histologically, these are all adenocarcinomas. There are some associated extracolonic neoplasms. Although a single dose of DMH produces tumors in some of the treated animals, the tumor yield on a weekly schedule is constant.38 It has been found that with increasing doses of DMH, the latency period in the colon is shortened and the yield in small bowel tumors is enhanced.35,39
Catalog of Herbs
Published in James A. Duke, Handbook of Medicinal Herbs, 2018
Toxicity — Cycasin is carcinogenic if orally administered to rats and pigs. With cattle neurotoxic effects are obvious. Other toxic symptoms include anemia, depression, diarrhea, jaundice, gastroenteritis, hemorrhage, nausea, coma, partial paralysis, and possibly death.33,56 Apparently it is mutagenic to onion root tip cells.33 Frequent use of the starch is suspected to cause cancer and hepatosis.56
Chemical Causes of Cancer
Published in Peter G. Shields, Cancer Risk Assessment, 2005
Gary M. Williams, Alan M. Jeffrey
Besides tissue biotransformation capabilities, the gastrointestinal tract contains organisms capable of a wide variety of chemical biotransformations (203,204). A classical example is the activation by bacteria of cycasin, the β-glycoside of methylazoxymethanol, which occurs in the cycad nut. Cycasin is only carcinogenic when hydrolyzed to the aglycone by bacterial gut flora. More recent studies have shown that bacterial gut flora are involved in the specific activation of several nitroarenes and more generally by causing enterohepatic circulation of conjugates excreted in the bile. In addition to their role in the overall biotransformation of potential carcinogens, bacteria also produce mutagens such as the fecapentaenes, which may act as promoters (205).
Lytico-bodig in Guam: Historical links between diet and illness during and after Spanish colonization
Published in Journal of the History of the Neurosciences, 2021
Santiago Giménez-Roldán, John C. Steele, Valerie S. Palmer, Peter S. Spencer
Those who do not subscribe to this view have pointed out that cycads have been used elsewhere for food, especially after typhoons have destroyed food crops, notably in the southern Nansei islands of Japan. However, a crucial difference is in the method of detoxication: Whereas on Guam, the seed gametophyte was soaked in water for highly variable periods, which resulted in concentrations of residual cycasin that were significantly associated with the incidence of ALS/PDC (Kisby, Ellison, and Spencer 1992; Román 1996), the Japanese method employed a fermentation step that destroyed all traces of cycasin (Kobayashi et al. 1974; Spencer 1990).
Capecitabine lipid nanoparticles for anti-colon cancer activity in 1,2-dimethylhydrazine-induced colon cancer: preparation, cytotoxic, pharmacokinetic, and pathological evaluation
Published in Drug Development and Industrial Pharmacy, 2018
Narendar Dudhipala, Goverdhan Puchchakayala
In this study, 1,2-dimethylhydrazine (DMH), a cycasin derivative, was used to induce colon cancer in rats [31]. DMH was dissolved in 1 mM EDTA just prior to use and the pH was adjusted to 6.5 with 1 mM NaOH to ensure the stability of the carcinogen. The rats were give intraperitoneal injection of DMH twice a week for two weeks at a dose of 30 mg/kg body weight [32,33].