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n dimethylnitrosamine/καρκινογένεση
Ο σύνδεσμος αποθηκεύεται στο πρόχειρο
Σελίδα 1 από 25 Αποτελέσματα
Identification of N5-methyl-N5-formyl-2,5,6-triamino-4-hydroxypyrimidine as a major adduct in rat liver DNA after treatment with the carcinogens, N,N-dimethylnitrosamine or 1,2-dimethylhydrazine.
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Σύνδεση εγγραφή
A major and previously undetected carcinogen-DNA adduct was found in the livers of rats given N,N-dimethylnitrosamine or 1,2-dimethylhydrazine. This adduct, which accounted for 55% of the total methyl residues in DNA at 72 hours after carcinogen treatment, was chromatographically identical to a
The formation and stability of methyl phosphotriesters in the DNA of rat tissues after treatment with the carcinogen N,N-dimethylnitrosamine.
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Following the injection i.p. of N,N-dimethylnitrosamine (DMN) into Chester Beatty (CB) hooded, female rats (2 mg/kg) measurable concentrations of methyl phosphotriesters were found in the DNA of liver, lung and kidney but not in spleen, thymus or brain. In lung and kidney these lesions were stable
The MR P-type transposable elements and the genetic activities of mutagens and carcinogens in Drosophila melanogaster. I. N,N-Dimethylnitrosamine (DMN).
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A technique was developed for the assay of the genetic activities of carcinogens in both the soma and germ line in the course of early larval development and to assess the extent of their modification through the introduction into the genome of the MR IInd autosome P-type transposable elements. The
Effects of the carcinogens N-methyl-N-nitrosourea and N-dimethylnitrosamine on spleen cell antigen binding in Xenopus laevis.
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A mutagenicity methodology for assessing the formation of N-dimethylnitrosamine in vivo.
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The mutagenicity test methodology in vitro has been extensively used during recent years in the identification of potential carcinogenic agents. Mutagenic analyses have been applied to the study of chemical reaction products for the demonstration of the formation of mutagenic agents. Recent studies
Nonlinear dose-response relationship for the binding of the carcinogen benzo(a)pyrene to rat liver DNA in vivo.
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With radioactive compounds of high specific activity, the binding of carcinogens to DNA can be measured with doses that are ineffective in long-term studies. The binding of tritiated benzo(a)pyrene to liver DNA of adult male rats has been determined 50 hr after a single i.p. injection of doses
Characterization of the purine ring-opened 7-methylguanine and its persistence in rat bladder epithelial DNA after treatment with the carcinogen N-methylnitrosourea.
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Purine ring-opened 7-methylguanine, prepared in vitro by alkaline treatment of 7-methylguanosine or of methylated calf thymus DNA, was extensively characterized by chromatographic and spectral techniques as N5-methyl-N5-formyl-2,5,6-triamino-4-hydroxypyrimidine. This modified base chromatographed as
Effect of treatment in vivo with N,N-dimethylnitrosamine or methyl methanesulphonate on the cytoplasmic DNA polymerase of regenerating rat liver.
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A 10-16 fold increase in rat liver cytoplasmic DNA polymerase (DNA polymerase-alpha) was observed by 24 hrs after two thirds partial hepatectomy. Injection of either N,N-dimethylnitrosamine (DMN) or methyl methanesulphonate (MMS) At 6 or 12 hrs after partial hepatectomy completely inhibited this
Urinary carcinogen [nitrosamine] production in a rat animal model for ureterosigmoidostomy.
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Tumor development at the site of ureterointestinal anastomosis is a recognized complication in patients undergoing ureterosigmoidostomy. In order to explore the hypothesis that carcinogens (nitrosamines) may be a factor in ureterosigmoidostomy, female Sprague-Dawley rats (n = 125) underwent urethral
Carcinogens in rubber production in the Soviet Union.
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In a preliminary phase of a broad research project on cancer among workers in a rubber footwear plant in Moscow, exposure to several known or potential carcinogens was assessed. There were high dust contents bearing both toxic substances and carcinogens. The highest concentrations of benzo[a]pyrene
Comparative studies of the hepatocarcinogen N,N-dimethylnitrosamine in vivo: reaction sites in rat liver DNA and the significance of their relative stabilities.
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The reaction of the hepatocarcinogen N,N-dimethylnitrosamine has been compared with that of methyl methanesulphonate, a methylating agent which is not a liver carcinogen. Consistent differences have been observed in the reaction of rat liver DNA in vivo with these agents; O(6)-alkylation and the
Transfer of methyl groups from N-dimethylnitrosamine to glycerolipids in rat liver.
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We have examined the in vivo labeling of lipids after a single intraperitoneal injection of the carcinogen, (C14) dimethylnitrosamine, into rats. Liver was most active in incorporating (C14) methyl groups into lipids (0.91% of the injected dose) and 80% of the activity appeared in
The effect of N-nitroso-N-methylurea and N-dimethylnitrosamine on cell mediated and humoral immune responses in rats and mice.
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N-Nitroso-N-methylurea (NMU) induced a marked dose dependent leucopoenia which was associated with an increased survival of skin allografts in adult rats and in 2 strains of mice. The humoral immune response to NMU as assessed by haemolytic plaque formation and haemagglutination was also much
Covalent binding of ethinylestradiol and estrone to rat liver DNA in vivo.
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The covalent binding of [6,7-3H] ethinylestradiol (EE) and [6,7-3H] estrone (E) to liver DNA of 200 g female rats was measured 8 h after the administration of 80 microgram (9.2 mCi) estrogen by gavage. The binding is 1.5 for EE and 1.1 for E, expressed as binding to DNA/dose, in units of mumol
Mutagenicities of N-nitrosamines on Salmonella.
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The mutagenic activities of 11 N-nitrosamines were tested using Salmonella typhimurium TA100 and TA98. All the carcinogenic N-nitrosamines were mutagenic on TA100 with a drug-activating system from the rat liver, whereas N,N-diphenylnitrosamine, a non-carcinogen, was not mutagenic. None of the
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