methylnitronitrosoguanidine and methylnitrosocyanamide
methylnitronitrosoguanidine has been researched along with methylnitrosocyanamide* in 4 studies
Other Studies
4 other study(ies) available for methylnitronitrosoguanidine and methylnitrosocyanamide
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Mode of mutagenic action of methylnitrosocyanamide, a potent carcinogen.
A potent carcinogen, methylnitrosocyanamide was used to induce revertants in a strain of Escherichia coli carrying an amber mutation in a gene for tryptophan (trp) biosynthesis and an ochre mutation in a gene for alkaline phosphatase biosynthesis. Trp+ revertants were purified and classified into seven categories based on their ability to support the growth of particular nonsense mutants of phage lambda and on their content of alkaline phosphatase. About 90% of the Trp+ revertants induced by methylnitrosocyanamide were due to mutations in suppressor genes, and 85% of the suppressor mutations occurred in gene supE. Intragenic reversion cannot occur by a GC leads to AT base substitution mutation, whereas this is the obligate mode of mutation in gene supE. We conclude that methylnitrosocyanamide preferentially induces GC leads to AT transition mutations but that other base substitution mutations are also induced at about 10% of this frequency. N-Methyl-N-nitrosourea and, particularly, N-methyl-N'-nitro-N-nitrosoguanidine also preferentially induce GC leads to AT transition mutations. Topics: Codon; Cyanamide; Escherichia coli; Methylnitronitrosoguanidine; Methylnitrosourea; Mutation; Nitrosamines; Suppression, Genetic | 1978 |
Chromosomal aberration, mutation and morphological transformation of Syrian hamster embryonic cells after exposure to methylnitrosocyanamide.
Hamster embryonic fibroblasts were treated directly with various concentrations of methylnitrosocyanamide (MNC), a nitrosated product of methylguanidine (MG) or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Then they were examined for chromosomal aberrations, morphological transformation and mutations resistant to 8-azaguanine (8AG) and 6-thioguanine (6TG). Direct treatment with 2 to 10 X 10(-6) M MNC caused a marked, dose-dependent appearance of 8AG- and 6TG-resistant mutations. The ability of MNC to induce mutations was similar to that of MNNG. Cultured embryonic fibroblasts in metaphase plates also showed a marked dose-dependent increase in chromosomal aberrations within 24 h after direct treatment with MNC or MNNG. Moreover, MNC and MNNG caused similar rates of morphological transformation. Topics: Animals; Azaguanine; Cell Line; Cell Transformation, Neoplastic; Chromosome Aberrations; Chromosomes; Cricetinae; Dose-Response Relationship, Drug; Drug Resistance; Guanidines; Mesocricetus; Methylguanidine; Methylnitronitrosoguanidine; Mutation; Nitrosamines; Thioguanine | 1977 |
Effect of methylnitrosocyanamide on cultured mammalian cells.
Effect of methylnitrosocyanamide (MNC) on a cultured mammalian cell line was examined in comparison with that of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). It was observed that MNC was about 3 times more potent than MNNG in the experiments on toxicity and inducibility of chromosome aberration and mutation. An increase in toxicity of MNNG was observed by minimizing the elevation of pH, while toxicity of MNC was more potent in the serum-free condition than in the presence of serum. Further, MNC was shown to be extremely rapid-acting, that is, 10 min was enough to exert its toxic effect. Topics: Cell Division; Cell Line; Chromosome Aberrations; Chromosomes; Methylnitronitrosoguanidine; Mutation; Nitrosamines | 1977 |
Mucosal damage induced by various gastric carcinogens in the glandular stomach of the rat.
The process of erosion formation in the glandular stomach of the rat given single and multiple intragastric doses of 100 mg N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)/kg body weight, was studied histologically, histochemically, and ultramicroscopically and compared with erosion induced by other gastric carcinogens and erosion-forming chemicals. The acute effect of several nongastric carcinogens on the glandular mucosa was also studied. The earliest degenerative transformation, fatty change, was found in the surface mucous cells within 1 hour a one-pulse intragastric dose of 100 mg MNNG/kg body weight; the change gradually progressed into deeper glandular cells and after three successive doses, erosion was complete in every rat. Ultrastructurally, four main glandular cells showed essentially similar degenerative alterations. Fatty change was also induced by other gastric caricnogens such as 4-nitroquinoline-1-oxide, methylnitrosocyanamide, methylnitrosourea, N-2-fluorenylacetamide, and iodacetamide, a noncarcinogenic alkylating agent. Mucosal damage induced by acetylsalicylic acid and thermal burn did not show fatty change. Nongastric carcinogens failed to induce mucosal damage. The relationship of the carcinogen-induced fatty change and mucosal damage to carcinogenesis was discussed. Topics: 2-Acetylaminofluorene; Animals; Endoplasmic Reticulum; Female; Gastric Mucosa; Iodoacetamide; Lipid Metabolism; Male; Methylnitronitrosoguanidine; Methylnitrosourea; Mucins; Nitroquinolines; Nitrosamines; Nitroso Compounds; Nitrosoguanidines; Rats | 1975 |