N-Nitroso-N-methylurea
(Synonyms: 1-甲基-1-亚硝基脲,NMU; MNU; NMH) 目录号 : GC39498
N-Nitroso-N-methylurea (NMU, MNU, NMH, 1-Methyl-1-nitrosourea, N-Methyl-Nnitrosourea, Methylnitrosourea) is a highly reliable carcinogen, mutagen, and teratogen.
Cas No.:684-93-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
N-Nitroso-N-methylurea (NMU, MNU, NMH, 1-Methyl-1-nitrosourea, N-Methyl-Nnitrosourea, Methylnitrosourea) is a highly reliable carcinogen, mutagen, and teratogen.
[1] N P Sen, et al. J Agric Food Chem . 2000 Oct;48(10):5088-96.
| Cas No. | 684-93-5 | SDF | |
| 别名 | 1-甲基-1-亚硝基脲,NMU; MNU; NMH | ||
| Canonical SMILES | O=C(N)N(C)N=O | ||
| 分子式 | C2H5N3O2 | 分子量 | 103.08 |
| 溶解度 | DMSO: 125 mg/mL (1212.65 mM) | 储存条件 | 4°C, protect from light, stored under nitrogen |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 9.7012 mL | 48.506 mL | 97.012 mL |
| 5 mM | 1.9402 mL | 9.7012 mL | 19.4024 mL |
| 10 mM | 0.9701 mL | 4.8506 mL | 9.7012 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Transnitrosation of non-mutagenic N-nitrosoproline forms mutagenic N-Nitroso-N-methylurea
Bioorg Med Chem 2015 Jul 1;23(13):3297-302.PMID:25975641DOI:10.1016/j.bmc.2015.04.058.
N-Nitroso-N-methylurea (NMU) is a potent carcinogen and suspected as a cause of human cancer. In this study, mutagenic NMU was detected by HPLC after the transnitrosation of non-mutagenic N-nitrosoproline (NP) to N-methylurea in the presence of thiourea (TU) under acidic conditions. The structure of NMU was confirmed by comparing (1)H NMR and IR spectra with that of authentic NMU after fractionation by column chromatography. Furthermore, a fraction containing NMU formed by transnitrosation was mutagenic in Salmonella typhimurium TA1535. NMU was formed in the reaction of NP and N-methylurea in the presence of 1,1,3,3-tetramethylthiourea (TTU) or 1,3-dimethylthiourea in place of TU as an accelerator. The reaction rate constants (k) for NMU formation were correlated with their nucleophilicity of sulfur atom in thioureas. The N-methylurea concentration did not affect the NMU formation, whereas the rate of NMU formation correlated linearly with concentrations of NP, TTU and oxonium ion. The observed kinetics suggests a mechanism by which the nitroso group was transferred directly from the protonated NP to the thiourea then to N-methylurea to form NMU. The rate-determining step was the formation of the complex with the protonated NP and thiourea.
N-Nitroso-N-methylurea elicits mammary cancer in resistant and sensitive rat strains
Proc Natl Acad Sci U S A 1981 Feb;78(2):1185-8.PMID:6785750DOI:10.1073/pnas.78.2.1185.
A single intravenous (i.v.) injection of the water-soluble mammary carcinogen N-Nitroso-N-methylurea (NMU; 35 mg/kg of body weight) elicited cancer of the breast in young female rats of two strains in the following incidence: Long-Evans strain, 4%; Sprague-Dawley strain, 70%. In sisters of these rats, a set of 5 i.v. injections of NMU (35 mg/kg at biweekly intervals) evoked mammary carcinoma as follows: Long-Evans strain, 76%; Sprague-Dawley strain, 100%. In its effectiveness in evoking mammary cancer in Sprague-Dawley rats, the lipid-soluble mammary carcinogen 7,8,12-trimethylbenz[a]anthracene exceeded NMU in rapidity of development of cancer and in tumor yield.
Effects of Lactofermented Beetroot Juice Alone or with N-Nitroso-N-methylurea on Selected Metabolic Parameters, Composition of the Microbiota Adhering to the Gut Epithelium and Antioxidant Status of Rats
Nutrients 2015 Jul 16;7(7):5905-15.PMID:26193312DOI:10.3390/nu7075260.
An objective of this work was to assess the biological activity of beetroot juice (Chrobry variety, Beta vulgaris L. ssp. vulgaris), which was lactofermented by probiotic bacteria Lactobacillus brevis 0944 and Lactobacillus paracasei 0920. The oxidative status of blood serum, kidneys, and liver of rats consuming the fermented beetroot juice were determined. The experimental rats were divided into four groups on diet type: Basal diet, basal diet supplemented with fermented beetroot juice, basal diet and N-Nitroso-N-methylurea treatment, and basal diet supplemented with fermented beetroot juice and N-Nitroso-N-methylurea treatment. Mutagen N-Nitroso-N-methylurea, which was added to diet in order to induce aberrant oxidative and biochemical processes and disadvantageous changes in the count and metabolic activity of the gut epithelium microbiota. The nutritional in vivo study showed that supplementing the diet of the rats with the lactofermented beetroot juice reduced the level of ammonia by 17% in the group treated with N-Nitroso-N-methylurea. Furthermore, the positive modulation of the gut microflora and its metabolic activity was observed in groups of rats fed with the diet supplemented with the fermented beetroot juice. A concomitant decrease in the b-glucuronidase activity was a consequence of the gut epithelium microbiota modulation. The antioxidant capacity of blood serum aqueous fraction was increased by about 69% in the group of rats treated N-Nitroso-N-methylurea mixed with the fermented beetroot juice and N-Nitroso-N-methylurea versus to the N-Nitroso-N-methylurea treatment, whereas the antioxidant parameters of the blood serum lipid fraction, kidneys, and liver remained unchanged.
Fluorometric determination of N-Nitroso-N-methylurea with nicotinamide and acetophenone
Anal Sci 2001 Mar;17(3):375-8.PMID:11990612DOI:10.2116/analsci.17.375.
A fluorometric method for the determination of N-Nitroso-N-methylurea (NMU) has been developed. It is based on the N-methylation reaction of nicotinamide with NMU and a subsequent condensation reaction with acetophenone, followed by an acid treatment to form a fluorescent 2,7-naphthyridine derivative. This method enabled the determination of NMU in the range 0.05 - 2 nmol/200 microl with a relative standard deviation of ca. 3%. It was applied to the determination of NMU formed from a precursor N-methylurea (MU) under simulated gastric conditions containing nitrite and thiocyanate ions at pH 3.0 in the presence of fresh orange juice and milk. NMU was extracted by an Extrelut 20 column and then determined. The mean recoveries of NMU added to the simulated gastric juice containing water, orange juice and milk were 86.5, 85.1 and 69.8%, respectively. The amounts of NMU formed from MU were found to decrease to below 25% in the presence of orange juice and milk.
N-nitroso-N-methylurea-induced rat mammary tumors arise from cells with preexisting oncogenic Hras1 gene mutations
Proc Natl Acad Sci U S A 1994 Apr 26;91(9):3749-53.PMID:8170982DOI:10.1073/pnas.91.9.3749.
GGA to GAA mutations in the 12th codon of the Hras gene are frequently observed in rat mammary tumors induced by N-Nitroso-N-methylurea (NMU). We developed an assay to measure point mutations present in tissues at a frequency of 10(-5) and have now applied this assay to measure the specific G to A transition of the Hras gene in rat mammary epithelium. We find that (i) 70% of untreated rats contain detectable levels of Hras mutants; (ii) these mutants are clustered within the gland as sectors in a manner consistent with their origin as a mutation arising during early organ development; and (iii) treatment with a carcinogenic dose of NMU did not result in a significant increase in the number of such mutants, the fraction of organ sectors with mutant cells, or the fraction of animals containing detectable levels of ras mutants. We conclude that the NMU-induced mammary tumors carrying the G to A transition at the 12th codon of the Hras gene arose from preexisting ras mutants and that an independent effect of NMU was directly or indirectly responsible for tumor formation.