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N-Nitroso-N-methylurea


CAS No. : 684-93-5

684-93-5
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Cat. No. : HY-34758
M.Wt: 103.08
Formula: C2H5N3O2
Purity: >98 %
Solubility: DMSO : 125 mg/mL (ultrasonic)
Introduction of 684-93-5 :

N-Nitroso-N-methylurea (NMU;MNU;NMH) is a potent carcinogen, mutagen and teratogenand. N-Nitroso-N-methylurea is a direct-acting alkylating agent that interacts with DNA. N-Nitroso-N-methylurea targets multiple animal organs to cause various cancer and/or degenerative disease. N-Nitroso-N-methylurea is also a precursor in the synthesis of diazomethane[1][2][3][4]. In Vitro:N-Nitroso-N-methylurea (NMU; 5 μM) treatment increases the cellular NF-κB activity in human malignant keratinocytes. N-Nitroso-N-methylurea also increases the amount of I-κBα phosphorylation[5]. In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

N-Nitroso-N-methylurea can be used in animal modeling to construct rat tumor models.

N-Nitroso-N-methylurea (NMU) gives intravenously to rats at age 50 days induced mammary carcinomas in 89% of BUF/N, 73% of Sprague-Dawley, and 89% of F344 females. Latent periods are, respectively, 77, 86, and 94 days. Doubling times of NMU-induced primary and transplanted carcinomas are similar to 7 days. Cachexia ensues at the 5th week from the onset of the first tumor. When the tumor is larger than 15 g, hypercalcemia is usually observed[1].

N-Methyl-N-nitrosourea (MNU) can be used to create models of gastric cancer and breast cancer[6][7].

Induction of Gastric Cancer[6]
Background
N-Methyl-N-nitrosourea (MNU) is a direct-acting alkylating agent that interacts with DNA. Accumulation of mutations may enhance cancer risk in target organs or cause cell death in susceptible tissues or cells when excessive DNA damage is not repaired. MNU targets various organs in a variety of animal species[2].
Specific Mmodeling Methods
Rat: albino Wistar • male • 5-6-week-old; 110-140 g
Administration: 100 mg/kg • ig • thrice in a week for 16 weeks
Note
(1) Dissolved in citrate buffer and 5% saline thrice in a week via intragastric route for 16 weeks.
(2) 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 week.
Modeling Indicators
Individual phenotypic changes: showed a significant decrease in body weight, water intake, and feed intake.
Molecular changes: increased the mean serum gastrin level, increased level of lipid peroxidation and decreased reduced glutathione level in gastric tissues.
Tissue changes: MNU-induced rats disclosed that the non-glandular stomach epithelium was hypertrophic with vacuolations and orthokeratotic hyperkeratosis after 16 wk of MNU induction but vacuolations and hyperkeartosis were not that much observed at 8 wk of MNU induction.

Induction of Breast Cancer[7]
Background
DNA Damage: After entering the body, MNU can be metabolically activated to form active nitrosyl compounds. These compounds react with DNA molecules, causing DNA strand breaks or base modifications, particularly alkylations such as O6-methylguanine. If not repaired, this type of damage can lead to mutations during cell division.
Gene Mutations: Due to the aforementioned DNA damage not being effectively repaired, errors may occur when cells replicate DNA, resulting in gene mutations. These mutations can affect key processes such as cell cycle regulation, apoptosis signaling pathways, and DNA repair mechanisms, thereby promoting tumor initiation and progression.
Uncontrolled Cell Proliferation: Gene mutations induced by MNU can activate oncogenes or inactivate tumor suppressor genes, disrupting normal cell growth control mechanisms. This results in cells losing their responsiveness to external growth inhibitory signals, leading to abnormal proliferation.
Pro-inflammatory Environment: Research has shown that MNU may also promote tumor development by altering the local microenvironment, such as increasing the expression of inflammatory factors. A chronic inflammatory state is considered an important factor in tumor development, as it can promote angiogenesis, epithelial-mesenchymal transition (EMT), and other processes that favor cancer progression.
Specific Modeling Methods
Rat: Albino Wistar • female • 35-day-old; 110-140 g
Administration: 50 mg/kg • ip • at 50, 65, and 80 days of age
Note
Modeling Indicators
Molecular changes: increased cyclin D1 expression, and showed p21Cip1 overexpression.
Tissue changes: observed breast tumors, and increased the mean volumes of tumors.

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