Blood flow rates were compared in non-inflamed and inflamed gingiva in 4 dogs following a depot injection of 133Xe and external monitoring of the radioisotope. Only teeth in the left jaws were cleaned daily and gingival health maintained. Selection of sites for testing was dependent on Gingival Index scores of 0 (no inflammation) or 2 (overt gingivitis). Measurements were made of 133Xe clearance from the interdental and attached gingiva and alveolar mucosa of the 2nd, 3rd and 4th premolars. Data were analysed using the initial slope clearance rate determination of Sejrsen and Tonnesen (1968) and the stochastic method of Zierler (1965) to determine a blood-flow-to-volume ratio. There was a significantly (p < 0.001) lower rate of clearance of 133Xe in alveolar mucosa compared to the other gingival sites, a difference not dependent on the presence of inflammation. There was no difference in 133Xe clearance rates in non-inflamed and inflamed gingiva. Thus the blood flow rate in the gingival nutritional capillary bed was maintained in chronically inflamed gingiva.

The formation of 7-methylguanine in rat liver mitochondrial DNA following the administration of the powerful carcinogen, dimethylnitrosamine, and the weak carcinogen, methyl methanesulphonate was measured and compared to the alkylation of nuclear DNA by these agents. At all doses tested mitochondrial DNA was alkylated more extensively than nuclear DNA by dimethylnitrosamine but both types of cellular DNA were alkylated to about the same extent by methyl methanesulphonate.

Single toxic doses of 1,2-dimethylhydrazine induced mild centrilobular necrosis of the liver in rats and mice. Ultrastructural studies showed hepatic nuclear changes including nucleolar microsegregation and changes in the endoplasmic reticulum and mitochondria. 1-Methylhydrazine caused little morphological change in the liver. Tumours of the colon and kidney and also massive cystic hyperplasia of the liver were found in some of the rats and tumours of the anal margin and kidney in some of the mice, following single doses of 1,2-dimethylhydrazine. Incorporation of amino acids into rat liver proteins was inhibited by 1,2-dimethylhydrazine, which also caused disaggregation of hepatic polysomes. No effects on hepatic protein synthesis by 1,1-dimethylhydrazine or 1-methylhydrazine were observed. Similarities between the effects of 1,2-dimethylhydrazine, cycasin and dimethylnitrosamine are discussed.

1,2-Dimethylhydrazine, in contrast to 1-methylhydrazine, is a potent carcinogen for the colon in rats and mice. 1,2-[14C]Dimethylhydrazine was administered to rats and mice in doses which are carcinogenic following a single dose in the former species, or carcinogenic on repeated administration in the latter species, and the rate of 14CO2 exhalation was measured. Exhalation of 14CO2 was also studied after administration of single doses of 1-[14C]methylhydrazine to mice. Incorporation of radioactivity into the nucleic acids of a variety of organs was found at a time after injection (about 6 h) when 14CO2 production from both compounds was virtually complete. Methylation of nucleic acids of liver and colon, as indicated by the formation of 7-methylguanine, was observed after treatment with 1,2-dimethylhydrazine and to a smaller extent by a factor of about 10 after treatment with 1-methylhydrazine. Less than 1% of a single dose of 1,2-[14C]dimethylhydrazine was excreted in the bile of rats as determined by chemical and radioactivity assays. The similarities of the biological and biochemical actions of 1,2-dimethylhydrazine with those of some nitroso compounds and of cycasin (methylazoxymethanol glucoside) are emphasized.

The mutagenic properties of hydrazine and its mono- and di-methyl derivatives were compared by direct microbial tests with the tryptophan auxotroph Escherichia coli as indicator organism. The methyl- and dimethyl-hydrazine were also tested with metabolic activation both by the Ames plate test and by the host-mediated assay with the histidine auxotroph Salmonella typhimurium tester strains. Only hydrazine and methylhydrazine were mutagenic in direct tests, hydrazine being a far more potent mutagen than methylhydrazine. Neither methylhydrazine nor dimethylhydrazines gave positive results in the Ames tests. In host-mediated assays, symmetrical dimethylhydrazine was clearly mutagenic, whereas methylhydrazine showed marginal mutagenic activity, and unsymmetrical dimethylhydrazine was negative. Evidently the mutagenic actions of different hydrazine derivatives, though these compounds are chemically closely related, depend on different reaction mechanisms.

Research Article| March 01 1971 Short Communications. Increased transfer ribonucleic acid methylase activity in tumours induced in the mouse colon by the administration of 1,2-dimethylhydrazine A E Pegg; A E Pegg Search for other works by this author on: This Site PubMed Google Scholar A Hawks A Hawks Search for other works by this author on: This Site PubMed Google Scholar Biochem J (1971) 122 (1): 121–123. https://doi.org/10.1042/bj1220121 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation A E Pegg, A Hawks; Short Communications. Increased transfer ribonucleic acid methylase activity in tumours induced in the mouse colon by the administration of 1,2-dimethylhydrazine. Biochem J 1 March 1971; 122 (1): 121–123. doi: https://doi.org/10.1042/bj1220121 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Journal Search Advanced Search This content is only available as a PDF. © 1971 London: The Biochemical Society1971 Article PDF first page preview Close Modal You do not currently have access to this content.

1. Administration of a large dose (500mg/kg body wt.) of (3)H-labelled l-ethionine to rats resulted in the incorporation of a small amount of radioactivity into the liver DNA. Considerable evidence that this radioactivity was not due to contamination of the isolated DNA with labelled protein, RNA, S-adenosyl-l-ethionine or l-ethionine was obtained. 2. After acidic hydrolysis of the DNA isolated from the livers of rats treated with labelled l-ethionine, virtually all of the radioactivity present in the DNA was found in a fraction with similar chromatographic properties to 7-ethylguanine. 3. Treatment of rats with comparable doses of l-methionine did not lead to the formation of 7-methylguanine in the liver DNA. 4. These results are discussed in relation to the induction of liver tumours by ethionine.