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dc.contributor.authorZaidi, N H
dc.contributor.authorO'Connor, Peter J
dc.date.accessioned2010-05-05T12:00:52Z
dc.date.available2010-05-05T12:00:52Z
dc.date.issued1995-03
dc.identifier.citationIdentification in rat stomach mucosae of a cell population characterized by a deficiency for the repair of O6-methyldeoxyguanosine from DNA. 1995, 16 (3):461-9 Carcinogenesisen
dc.identifier.issn0143-3334
dc.identifier.pmid7697799
dc.identifier.doi10.1093/carcin/16.3.461
dc.identifier.urihttp://hdl.handle.net/10541/97939
dc.description.abstractImmunohistochemical studies have been used to show the time course for the cell-specific methylation of DNA in the upper gastrointestinal tract of rats treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The doses used were 1, 5, 25 and 50 mg MNNG/kg (i.g.) and tissue samples were analysed at intervals of from 1 to 192 h after treatment. Relatively little reaction with nuclear DNA was observed in the forestomach and still less in the oesophagus. Reaction with DNA was most extensive in the corpus, pylorus and the duodenum, reaching a peak of staining intensity between 2 and 4 h and then declining progressively there-after. Staining for the presence of O6-methyldeoxyguanosine (O6-MedG) in DNA was highly selective and tended to occur in the nuclei of the basal cell of the oesophagus and forestomach and in the cells of the lumenal border of the glands and villi of the corpus, pylorus and duodenum. There were also areas, 5-15, glands apart where staining for O6-MedG in the corpus and pylorus extended as far down as the basal mucosa. From 12 h after MNNG treatment, in the corpus and pylorus, a band of strongly methylated cells became apparent about 3-6 cells deep from the lumen and remained identifiable up to 168 h after treatment with the higher doses. These cells, which apparently have a very low O6-MedG repair capacity, are stationary (i.e. not part of the escalator) and are located in the mesenchymal tissue elements as demonstrated by staining of serial sections with cytokeratin or vementin. The significance of this population of cells is unknown.
dc.language.isoenen
dc.subject.meshAnimals
dc.subject.meshCarcinogens
dc.subject.meshDNA
dc.subject.meshDNA Repair
dc.subject.meshDeoxyguanosine
dc.subject.meshDuodenum
dc.subject.meshGastric Mucosa
dc.subject.meshImmunohistochemistry
dc.subject.meshMale
dc.subject.meshMethylation
dc.subject.meshMethylnitronitrosoguanidine
dc.subject.meshMethylnitrosourea
dc.subject.meshRats
dc.subject.meshRats, Wistar
dc.titleIdentification in rat stomach mucosae of a cell population characterized by a deficiency for the repair of O6-methyldeoxyguanosine from DNA.en
dc.typeArticleen
dc.contributor.departmentCancer Research Campaign Department of Carcinogenesis, Paterson Institute for Cancer Research, Christie Hospital (NHS Trust), Manchester, UK.en
dc.identifier.journalCarcinogenesisen
html.description.abstractImmunohistochemical studies have been used to show the time course for the cell-specific methylation of DNA in the upper gastrointestinal tract of rats treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The doses used were 1, 5, 25 and 50 mg MNNG/kg (i.g.) and tissue samples were analysed at intervals of from 1 to 192 h after treatment. Relatively little reaction with nuclear DNA was observed in the forestomach and still less in the oesophagus. Reaction with DNA was most extensive in the corpus, pylorus and the duodenum, reaching a peak of staining intensity between 2 and 4 h and then declining progressively there-after. Staining for the presence of O6-methyldeoxyguanosine (O6-MedG) in DNA was highly selective and tended to occur in the nuclei of the basal cell of the oesophagus and forestomach and in the cells of the lumenal border of the glands and villi of the corpus, pylorus and duodenum. There were also areas, 5-15, glands apart where staining for O6-MedG in the corpus and pylorus extended as far down as the basal mucosa. From 12 h after MNNG treatment, in the corpus and pylorus, a band of strongly methylated cells became apparent about 3-6 cells deep from the lumen and remained identifiable up to 168 h after treatment with the higher doses. These cells, which apparently have a very low O6-MedG repair capacity, are stationary (i.e. not part of the escalator) and are located in the mesenchymal tissue elements as demonstrated by staining of serial sections with cytokeratin or vementin. The significance of this population of cells is unknown.


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