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Experimental Lung Carcinogenesis by Intravenous Administration
Published in Joan Gil, Models of Lung Disease, 2020
N-nitroso-n-methylurea (NMU) was examined for its carcinogenicity by IV administration in many animal species, including mouse, rat, hamster, gerbil, rabbit, dog, and monkey. In mice treated with IV administration of NMU, tumors developed in the lung as well as in the stomach, liver, lymphoid organs, and brain (Denlinger et al., 1974). The IV administration of NMU to other species induced tumors at multiple sites, especially in the nervous tissues (Druckrey et al., 1967; IARC monographs, 1978).
Estrogens, Xenoestrogens, and the Development of Neoplasms
Published in Rajesh K. Naz, Endocrine Disruptors, 2004
Endometrial tumors occur at a relatively high incidence in certain strains of rats. DES exposure throughout adult life results in a 1.7% incidence of uterine adeno carcinoma in mice, while neonatal (day 1 to5) administration results in 90% incidence. Tumors did not develop in animals ovariectomized before puberty.144 These tumors required estrogens for continuous growth when transplanted. Adenocarcinomas of the uterus may also be developed by administration of the carcinogen n-nitroso-n-methylurea (NMU) to intact adult mice.163 Progestagens inhibited the development of tumors in estrogen-treated animals.164
Recent progress in the development of small molecule Nrf2 activators: a patent review (2017-present)
Published in Expert Opinion on Therapeutic Patents, 2020
Haishan Zhou, Yan Wang, Qidong You, Zhengyu Jiang
Patent CN106265633 by Wang et al. [80] reported the atractylenolide II (21) could treat and prevent the diseases associated with Nrf2 pathway. In vitro, 21 remarkably activated Nrf2 and increased the expression of its downstream antioxidative enzymes (HO-1 and NQO1), so that protected against LPS-induced inflammation and oxidative stress. Further research showed the cytoprotective effects of 21 were related to a c-Jun N-terminal kinase (JNK)/extracellular signal-regulated kinase (ERK)-Nrf2-ARE-dependent manner. In vivo, 21 significantly promoted mRNA and protein levels of Nrf2 and its downstream antioxidative enzymes in N-Nitroso-N-methylurea-induced rats. 21 showed protective effects against mammary tumorigenesis by reducing tumor incidence, multiplicity, and volume, and decreasing inflammation and oxidative stress in rat mammary tissue.
Palliative Role of Aqueous Ginger Extract on N-Nitroso-N-Methylurea-Induced Gastric Cancer
Published in Nutrition and Cancer, 2020
Debjani P. Mansingh, Shalini Pradhan, Deeptarup Biswas, R. Barathidasan, Hannah R. Vasanthi
Although various animal models exist for gastric cancer such as induction with N-nitrosodiethylamine, N-methyl-N-nitro-N-nitrosoguanidine, Benzo[a]pyrene, N-Nitroso-N-methylurea, and genetic models C57BL/6J, C3H/HeN, and Sprague dawley rats to screen anticancer drugs, still they are encountered with some limitations. N-methyl-N-nitrosourea, an alkylating agent and a N-nitroso compound that induces mutation specifically through AT:GC transition, is considered as the best characterized model for chemical induced gastric cancer (11). Induction of gastric carcinomas by N-Nitroso-N-methylurea (MNU) in male rats is one of the most frequently used animal models for the investigation of stomach carcinogenesis and tumor treatment due to the several advantages it possesses, such as reliability of tumor induction, organ site specificity, and predominantly carcinomatous histopathologic characterization. Herein, male albino Wistar rats were equally randomized in to 2 groups of twelve animals each: Normal control rats (Group I) were fed with 1 ml of citrate buffer (pH – 4.5) orally and normal saline (1 ml/rat) thrice a week throughout the experiment (8 and 16 wks. Cancer-control rats (Group II) were administrated with MNU (100 mg/kg b.w.) in citrate buffer, pH – 4.5 and normal saline thrice in a week via intragastric route. The optimum dose for MNU was selected from the previous literature (12). Initially, MNU was administered (n = 6) for a period of 8 wk and then continued till 16 wk (n = 6) to check the extent of carcinogenicity as part of our standardization protocol. Weekly body weight was measured to check the health status as well as the induction of cancer, whereas feed intake and water intake were measured daily to check the routine metabolic activities of the experimental animals. The level of cancer induction was identified by specific biochemical markers such as serum gastrin level, TBARS, and glutathione followed by histopathological analysis at two-time periods for 8 and 16 wk.