Disease relevance of Methyldimethylaminoazobenzene

• The chronobiology of ornithine decarboxylase (ODC) activity in livers was investigated in noninbred Sprague-Dawley rats fed for 5 months with a basal diet or diets with 3-methyl-4'-(dimethylamino)azobenzene (3-Me-DAB) that were oncogenic or caused bile duct hyperplasia (1-naphthylisothiocyanate) (NIT) [1].
• Appearance of intestinal type of tumor cells in hepatoma tissue induced by 3'-methyl-4-dimethylaminoazobenzene [2].
• The changes in glycosaminoglycans in livers of rats with 3'-methyl-4-dimethylaminoazobenzene-induced hepatic cancer were examined and compared with those in fetal liver [3].
• Distribution of transglutaminase activity was determined in normal rat liver, a 3'-methyl-4-dimethylaminoazobenzene-induced primary hepatoma, and the Novikoff hepatoma [4].
• The early target Mr 14,000 protein of the carcinogen in normal rats was identified as being liver fatty acid-binding protein and was associated in hepatocytes with normal mitosis and the cell proliferation brought about by either of the two liver carcinogens, FAA or 3'-methyl-4-dimethylaminoazobenzene [5].

High impact information on Methyldimethylaminoazobenzene

• N-Benzoyloxy-3'-methyl-4-methylaminoazobenzene-(N-benzoyloxy-3'-Me-MAB) was highly toxic to rat liver epithelial cells (Ac2F) and induced many more chromosome aberrations and unscheduled DNA synthesis than did 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) [6].
• This time trend of hemodynamics and mitochondrial functions were studied to determine whether the ligation of the hepatic artery would result in an antitumor effect on 3'-methyl-4-dimethylaminoazobenzene-induced hepatic carcinoma in rats [7].
• The level of immunohistochemically albumin-positive hepatocytes is about 1 per 10(5) cells in neonatal NARs, increases with age, and further increases with chronic oral treatment with 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB) [8].
• DRH strain rats were established by inbreeding a closed colony of Donryu rats continuously fed the chemical hepatocarcinogen 3'-methyl-4-dimethylaminoazobenzene for over 10 years [9].
• Hepatomas were induced in rats by 0.06% 3'-methyl-4-dimethylaminoazobenzene [10].

Chemical compound and disease context of Methyldimethylaminoazobenzene

• Expression of non-hepatic-type S-adenosylmethionine synthetase isozyme in rat hepatomas induced by 3'-methyl-4-dimethylaminoazobenzene [11].
• Chromatography on AH-Sepharose 4B of the membrane sialidases of rat primary hepatoma induced by 3'-methyl-4-dimethylaminoazobenzene (MeDAB) further revealed that hepatocarcinogenesis induces a marked decrease in sialidase II but no decrease in sialidase I [12].
• A more striking elevation in tyrosine protein kinase activity is noted in rat hepatomas induced by administration of chemical carcinogens, in particular that of 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) [13].
• Low frequency of ras activation in 2-acetylaminofluorene- and 3'-methyl-4-(dimethylamino)azobenzene-induced rat hepatocellular carcinomas [14].
• Glycopeptide and glycosaminoglycans in the process of hepatic cancer induced by 3'-methyl-DAB [15].

Biological context of Methyldimethylaminoazobenzene

• The DNA content and ploidy state of cells isolated from the livers of rats exposed to the carcinogen 3'-methyl-4-dimethylaminoazobenzene for 10 and 20 weeks, as determined by flow cytometry, were correlated with the development of oval cells in the livers of treated animals and with serum levels of the oncoprotein alpha-fetoprotein (AFP) [16].
• A reduction in the ratio of tetraploid to diploid liver nuclei has been investigated as an early indicator of hepatocarcinogenesis in the rat using the liver carcinogen 3'-methyl-4-dimethylaminoazobenzene (3'M) [17].
• Metabolic activation of the hepatocarcinogen 3'-methyl-4-dimethylaminoazobenzene by a rat liver cell-free system. Evidence suggesting the formation of at least two electrophilic metabolites [18].
• Analyses of oxidative DNA damage and its repair activity in the livers of 3'-methyl-4-dimethylaminoazobenzene-treated rodents [19].
• The effect of the carcinogen 3'-methyl-4-dimethylaminoazobenzene (3'-MDAB) on the gene expression of rat liver was studied [20].

Anatomical context of Methyldimethylaminoazobenzene

• Comparative study of the phospholipid composition of plasma membranes isolated from rat primary hepatomas induced by 3'-methyl-4-dimethylaminoazobenzene and from normal growing rat livers [21].
• Binding of 3'-methyl-N,N-dimethyl-4-aminoazobenzene metabolites to rat liver cytosol proteins and ligandin subunits [22].
• Changes in peroxisomes in preneoplastic liver of rats induced by 3'-methyl-4-dimethylaminoazobenzene [23].
• The activities of these enzymes were also assayed in a fairly fast-growing, 3'-methyl-4-dimethylaminoazobenzene-induced transplantable rat hepatoma and in hepatoma cell lines derived from both rat and human tumors [24].
• Roles of ovaries and testes in hepatocellular tumorigenesis induced in mice by 3'-methyl-4-dimethylaminoazobenzene [25].

Associations of Methyldimethylaminoazobenzene with other chemical compounds

• Effect of phenobarbital administration on hepatocytes constituting the hyperplastic nodules induced in rat liver by 3'-methyl-4-dimethylaminoazobenzene [26].
• Continued ingestion of any of the three hepatocarcinogens, FAA, 3'-methyl-4-dimethylaminoazobenzene, or ethionine, resulted in the progressive loss of the early radioactive complex and the concurrent gain in liver cytosol of the late carcinogen: protein complex (Mr approximately 150,000) formed by the tracer dose of FAA [5].
• The DNA from spontaneous tumors of genetic origin in C3H mice and also from acetylaminofluorene, chlordane, or 3'-methyl-4-dimethylaminoazobenzene-induced tumors in C57Bl and B6C3 mice was undermethylated compared to the levels in background and normal liver samples [27].
• Changes in basal activity and hormone-responsiveness of adenylate cyclase were demonstrated in plasma membranes and intact cells from pre-cancerous liver of rats fed a diet containing the carcinogen 3'-methyl-4-dimethylaminoazobenzene [28].
• Effects of a protein-bound polysaccharide from a basidiomycetes against hepatocarcinogenesis induced by 3'-methyl-4-dimethylaminoazobenzene in rats [29].

Gene context of Methyldimethylaminoazobenzene

• Primary cultures of oval cells isolated from 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) treated rat liver (an enriched source of biliary epithelial cells) contained CK14 mRNAs which were slightly shorter than those in LECs [30].
• We investigated whether the antitumor action of sodium 5,6-benzylidene-L-ascorbate (SBA) is mediated via oxidation-involved mechanism, in three different systems: 3'-methyl-4-dimethylaminoazobenzene (DAB)-induced rat hepatocellular carcinoma (in vivo), its homogenate (semi in vivo), and cultured cells (in vitro) [31].
• Immunofluorescent study on alpha-fetoprotein-producing cells in the early stage of 3'-methyl-4-dimethylaminoazobenzene carcinogenesis [32].
• Histochemical and cytochemical study of butyrylcholinesterase activity in rat hepatocellular carcinomas induced by 3'-methyl-4-dimethylaminoazobenzene [33].
• The activity of butyrylcholinesterase (BCHE), a liver fetal isozyme (Zone L-V) of a nonspecific esterase, was studied histochemically and cytochemically in rat hepatocellular carcinomas induced by 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) [33].

Analytical, diagnostic and therapeutic context of Methyldimethylaminoazobenzene

• The effect of portacaval shunt on hepatocarcinogenesis was studied in rats fed 3'-methyl-4-dimethylaminoazobenzene [34].
• The various liver cell populations emerging during the transitory reappearance of alpha-fetoprotein (AFP) in serum of 3'-methyl-4-dimethylaminoazobenzene-ingesting rats were analyzed in situ and in vitro on isolated cell preparations in terms of their cytokeratin and AFP expression using single and double indirect immunofluorescence microscopy [35].
• The first ODC activity peak occurred 20 h after treatment with 3'-methyl-4-(dimethylamino)azobenzene (MDAB), at the same time that accumulation of the ODC-mRNAs was maximum [36].
• Ovariectomy at 1 month of age promotes development of hepatocellular adenomatous nodules in female C57BL/6 x DS-F1 mice treated neonatally with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) [37].
• Expressions of the c-Ha-ras and c-myc genes were studied by Northern blotting of total RNA from primary tumors and non-tumorous parts of the liver of rats given diet containing 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) and from established rat hepatoma cell lines [38].

References