Methylnitronitrosoguanidine(wetted with ca. 50% Water)
(Synonyms: 1-甲基-3-硝基-1-亚硝基胍,MNNG) 目录号 : GC36598
甲基亚硝基胍 (MNNG) 是一种具有口服活性的烷化剂，具有毒性和致突变作用。
Cas No.:70-25-7
Sample solution is provided at 25 µL, 10mM.
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- Purity: >95.00%
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| Cell experiment [1]: | |
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Cell lines |
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Preparation Method |
OC3 cells at passage 24 (OC3-P24) were treated with the carcinogen Methylnitronitrosoguanidine (MNNG, final concentration 3 µg/mL in medium) and protected from light. After 24 h, the media containing MNNG was removed and cells were rinsed 3 times with phosphate buffered saline (PBS). The process was repeated 15 times and cells were then cultured in regular medium and passaged when necessary. The induced cell line was designated as OC3W3-15, and it corresponds to regular cultured passage 38 of OC3 cells (OC3-P38) which served as control. Cell growth and morphology of both cell lines were regularly monitored with an inverted microscope. The ultrastructural changes during transformation were observed under the H-600 transmission electronic microscope (TEM). |
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Reaction Conditions |
3 µg/mL, 24 hours for 15 times |
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Applications |
After treatment with the carcinogen Methylnitronitrosoguanidine 15 times, the OC3W3-15 took on a long- or short-fusiform shape in a multilayer, overlapping and in a confused arrangement. The cells showed karyokinesis or even abnormal karyokinesis. |
| Animal experiment [2]: | |
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Animal models |
Male Wistar albino rats |
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Preparation Method |
Control rats were assisted for group I for 20 weeks. Group II was stimulated oral gave administration of MNNG (200 mg/kg bw) at 0 and 14th days. 1 ml of NaCl for each rats was given trice a day for 6 weeks for saturation and kept till the experimental period. Group III were stimulated with MNNG + Corilagin (30 mg/kg bw) and treated for 20 weeks with effective dosage. Corilagin (30 mg/kg bw) alone was taken as group IV. The experiment was carried out for 20 weeks and all the animals were sacrificed by cardiac puncture. |
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Dosage form |
Oral, 200 mg/kg, 2 weeks. |
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Applications |
In group II, the rat body weights were significantly decreased compared with normal group whereas, tumor weight was increased and also 100% gastric cancer incidence rats were also recorded. The rat body weight was increased and tumor weights significantly decreased in corilagin administered group compared to group II. |
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References: [1]: Ding L, Ding Y N, Lin Y, et al. Proteins related to early changes in carcinogenesis of hepatic oval cells after treatment with methylnitronitrosoguanidine[J]. Experimental and Toxicologic Pathology, 2014, 66(2-3): 139-146. |
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Methylnitronitrosoguanidine (MNNG) is an orally active alkylating agent, shows toxic and mutagenic effects. Methylnitronitrosoguanidine often used as carcinogen and mutagen in vivo and in vitro [1,2]. The MNNG mechanism of action is owing to its electrophilic compound degradations, where ammonium ion is the mutagen and leads to the electrophilic impact on DNA base pairs specifically on its nucleophilic sites [3].
After Methylnitronitrosoguanidine (3 µg/mL) treatment, the ultrastructure of the OC3W3-15 cells possessed larger nuclei with enlarged and prominent nucleoli, usually more than 2 in number. The amount of heterochromatin decreased while euchromatin increased. The cytoplasm was filled with abundant rough endoplasmic reticulum, free ribosomes, Golgi apparatus, and well-developed mitochondria, yet the nuclear-to-cytoplasmic ratio remained high [2]. Methylnitronitrosoguanidine (3 µg/mL) treatment increased proliferative rate of hepatic oval cells, and more cells were in prophase for rapid proliferation than in the control group [2]. 2×10-4 mol/L Methylnitronitrosoguanidine could increase the proliferation, promote the invasion and migration, suppress the apoptosis of GES-1 cells. The expression levels of NF-κB p65 mRNA and protein were upregulated in GES-1 cells after treatment with MNNG [4].
Methylnitronitrosoguanidine (200 mg/kg, 2 weeks) treatment significantly decreased the Male Wistar albino rats body weights, increased tumor weight and gastric cancer was induced in 100% of the rats [1]. Methylnitronitrosoguanidine (200 mg/kg, 2 weeks) reduced protein levels of Bax, caspase-3, and -9 [1].
References:
[1]. Zhang L, Jia B, Velu P, et al. Corilagin induces apoptosis and inhibits HMBG1/PI3K/AKT signaling pathways in a rat model of gastric carcinogenesis induced by methylnitronitrosoguanidine[J]. Environmental Toxicology, 2022, 37(5): 1222-1230.
[2]. Ding L, Ding Y N, Lin Y, et al. Proteins related to early changes in carcinogenesis of hepatic oval cells after treatment with methylnitronitrosoguanidine[J]. Experimental and Toxicologic Pathology, 2014, 66(2-3): 139-146.
[3]. Zhu, F., Xu, Y., Pan, J., Li, M., Chen, F., & Xie, G. (2021). Epigallocatechin gallate protects against MNNG-induced precancerous lesions of gastric carcinoma in rats via PI3K/Akt/mTOR pathway. Evidence-Based Complementary and Alternative Medicine, 2021.
[4]. XU J, ZHANG X, SUN D, et al. Effect of methylnitronitrosoguanidine (MNNG) on the malignant transformation of human gastric mucosa GES-1 cells and its mechanism[J]. Medical Journal of Chinese People's Liberation Army, 2016, 41(11): 887-891.
甲基亚硝基胍 (MNNG) 是一种具有口服活性的烷化剂,具有毒性和致突变作用。甲基亚硝基胍常被用作体内外致癌物和诱变剂[1,2]。 MNNG 的作用机制是由于其亲电化合物降解,其中铵离子是诱变剂,导致对 DNA 碱基对的亲电影响,特别是在其亲核位点 [3]。
在甲基亚硝基胍 (3 µg/mL) 处理后,OC3W3-15 细胞的超微结构具有较大的细胞核,核仁增大且突出,通常数量超过 2 个。异染色质减少而常染色质增加。细胞质中充满了丰富的粗面内质网、游离核糖体、高尔基体和发育良好的线粒体,但核质比仍然很高[2]。甲基亚硝基胍(3 µg/mL)处理提高了肝卵圆细胞的增殖率,并且比对照组有更多的细胞处于快速增殖的前期[2]。 2×104 mol/L Methylnitronitrosoguanidine可促进GES-1细胞增殖,促进侵袭和迁移,抑制细胞凋亡。 MNNG[4]处理后GES-1细胞NF-κB p65 mRNA和蛋白表达上调。
甲基亚硝基胍（200 mg/kg, 2周)治疗显着降低了雄性 Wistar 白化大鼠的体重,增加了肿瘤重量,并且在 100% 的大鼠中诱发了胃癌 [1]。甲基亚硝基胍（200 mg/kg,2 周）降低 Bax、caspase-3 和 -9 的蛋白质水平[1]。
| Cas No. | 70-25-7 | SDF | |
| 别名 | 1-甲基-3-硝基-1-亚硝基胍,MNNG | ||
| Canonical SMILES | N=C(N[N+]([O-])=O)N(C)N=O | ||
| 分子式 | C2H5N5O3 | 分子量 | 147.09 |
| 溶解度 | DMSO : 125 mg/mL (849.82 mM) | 储存条件 | Store at -20°C,unstable in solution, ready to use. |
| 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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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 6.7986 mL | 33.9928 mL | 67.9856 mL |
| 5 mM | 1.3597 mL | 6.7986 mL | 13.5971 mL |
| 10 mM | 0.6799 mL | 3.3993 mL | 6.7986 mL |
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| 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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2.
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Corilagin induces apoptosis and inhibits HMBG1/PI3K/AKT signaling pathways in a rat model of gastric carcinogenesis induced by methylnitronitrosoguanidine
Gastric cancer, invasive cancer of the gastrointestinal tract, found in developing countries. Chemotherapy to patients with advanced gastric cancer, exhibits greater drug resistance to standard chemotherapy drugs. Therefore, important to establish anti-cancer drugs that are successful for cancer therapy. Corilagin is a natural ellagitannin (ET) with profound pharmacological properties has been used for the study to assess its anticancer effects against N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) stimulated gastric cancer rats. Biochemical studies showed Thiobarbituric acid reactive substances (TBARS) and enzymatic and non-enzymatic antioxidants increased in corilagin treated animals compared with controls. Histopathologic evaluation revealed corilagin treated rats showed cell morphology similar that control showing its ameliorating effects. In corillagen treament mRNA protein expression levels of HIF-1α, AKT, PI3K, CT4, CD147 and HMGB1 were drastically lowered transcription factors triggering gastric cancer. In Western blot analysis showed released higher apoptotic marker of caspase-3, -9, Bax while Bcl-2 levels were significantly reduced confirming that corilagin triggers apoptosis in gastric cancer.
Effect of selenomethionine on N-methylnitronitrosoguanidine-induced colonic aberrant crypt foci in rats
An association between low selenium intake and the incidence or prevalence of cancers is well known. Selenium in the form of selenomethionine supplemented in drinking water has been found to be highly effective in reducing tumour incidence and preneoplastic foci during the development of hepatocarcinogenesis in rats in our previous studies. Here, an attempt has been made to investigate whether the dose and form of selenium found to be effective during hepatocarcinogenesis is equally effective in N-methylnitronitrosoguanidine-induced colorectal carcinogenesis in terms of antioxidant defence enzyme systems, DNA chain breaks and incidences of aberrant crypt foci. Treatment with selenomethionine either on initiation or on selection/promotion, or during the entire experiment showed that selenomethionine was most effective in regulating the cellular antioxidant defence systems, DNA chain break control and reducing aberrant crypt foci in the colorectal tissues of rats. Our results also confirm that selenium is particularly effective in limiting the action of the carcinogen during the initiation phase of this colorectal carcinogenesis, just as we found with hepatocarcinogenesis in our previous studies.
N-methyl-N'-nitro-N-nitrosoguanidine
N-Methyl-N'-nitro-N-nitrosoguanidine
Comparison of toxicity and mutagenicity of methylnitrosourea, methylnitronitrosoguanidine and ICR-191 among human lymphoblast lines
The toxic and mutagenic effects of the alkylating agents methylnitrosourea (MNU) and methylnitronitrosoguanidine (MNNG) and of the frameshift mutagen, ICR-191 were compared among 3 human diploid lymphoblast lines, MIT-2, WI-L2 and GM 130. The MIT-2 and WI-L2 lines were both sensitive to the toxic and mutagenic effects of all 3 agents tested. The WI-L2 line was more sensitive to the toxic effects of MNU and MNNG than the MIT-2 line, while it was somewhat less sensitive to the mutagenic effects of these alkylating agents. The GM 130 line was strikingly resistant to both the toxic and mutagenic effects of the alkylating agents. The order of sensitivity to the toxic effect of ICR-191 was MIT-2 greater than WI-L2 greater than GM 130, while the order of sensitivity to the mutagenic effects of this frameshift mutagen was GM 130 greater than MIT-2 greater than WI-L2. These results point to the importance of accounting possible variations in mutability among individuals when extrapolating from any single mutagenicity assay for human risk assessment.