Disease relevance of Butter Yellow

• Effects of aliphatic aldehyde metabolism on protein synthesis and thiol compounds in rat liver and hepatoma induced by 4-dimethylaminoazobenzene [1].
• A large increase in diamine oxidase activity, as compared to the values of normal liver, was also observed in 4-dimethylaminoazobenzene and Yoshida ascites hepatomas [2].
• The decrease of liver weight that occurred in shunted rats without loss of body weight produced a very significant reduction of the total capacity of liver to activate 4-dimethylaminoazobenzene while the total capacity of detoxification remained unchanged [3].
• An immunoperoxidase-staining technique was used to examine the distribution of determinants detected by these antibodies on frozen sections of fetal, neonatal, adult, and regenerating liver and on a range of 4-dimethylaminoazobenzene-induced liver lesions, including a panel of 32 primary liver carcinomas [4].
• Comparative mutagenicity of dimethylaminoazobenzene and analogues in Salmonella [5].

Psychiatry related information on Butter Yellow

• To document the long-term effect of TMX in mice treated with p-dimethylaminoazobenzene (DAB), we have investigated the time response action of these drugs on different biochemical parameters [6].

High impact information on Butter Yellow

• Detection of carcinogen-induced stimulation of cytochrome P-448-associated enzymes by 14CO2 breath analysis studies using dimethylaminoazobenzene [7].
• Infant male Fischer rats were much less susceptible; less than 25% of the rats given 4 i.p. injections (0.3 to 0.4 mumol/g of body weight/injection) of N-methyl-4-amino-azobenzene and less than or equal to 5% of those given these doses of N,N-dimethyl-4-aminoazobenzene or AB before 22 days of age developed hepatic carcinomas by 24 months [8].
• Diamine oxidase activity in regenerating rat liver and in 4-dimethylaminoazobenzene-induced and Yoshida AH 130 hepatomas [2].
• N-Benzoyloxy-N-methyl-4-aminoazobenzene, a synthetic model ultimate carcinogenic derivative of N-methyl- and N,N-dimethyl-4-aminoazobenzene, reacted with [8-14C]deoxyguanosine in vitro to yield ten 14C-containing products separable by high-performance liquid chromatography [9].
• Adducts from the reaction of N-benzoyloxy-N-methyl-4-aminoazobenzene with deoxyguanosine or DNA in vitro and from hepatic DNA of mice treated with N-methyl- or N,N-dimethyl-4-aminoazobenzene [9].

Chemical compound and disease context of Butter Yellow

• The concentrations of putrescine, spermidine, and spermine in liver of rats fed on 4-dimethylaminoazobenzene and in the resultant hepatomas were found to be significantly higher than were those observed in normal liver from rats of the same strain, sex, and age [10].
• A previously uncharacterized glutathione (GSH) transferase which is not apparent in normal liver, accounts for at least 25% of the soluble GSH transferase content of primary hepatomas induced by feeding N,N-dimethyl-4-aminoazobenzene [11].
• Inhibition of subcutaneous tumour growth, following treatment with tilorone hydrochloride, was observed with two transplantable methylcholanthrene-induced rat sarcomas (Mc7, Mc4), but similar drug treatment was ineffective against two rat hepatomas induced by dimethylaminoazobenzene (D23, D30) [12].

Biological context of Butter Yellow

• Stereological analysis of liver nodules and estimations of their size distribution demonstrated a significative enhancing effect of HBV transgene in both NDEA- and DAB-induced hepatocarcinogenesis in male mice [13].
• Its complete amino acid sequence was determined by manual degradation using a 4-dimethylaminoazobenzene 4'-isothiocyanate double-coupling method [14].
• In conclusion, although cimetidine treatment partially prevented and reversed cytochrome P450 induction, and alteration on haem metabolism provoked by p-dimethylaminoazobenzene AB, it did not reverse liver damage or lipid peroxidation [15].
• The rodent hepatocarcinogen p-dimethylaminoazobenzene induced colon DNA damage at 1 mg/kg, whereas it damaged liver DNA only at 500 mg/kg [16].
• Regulation of thiol environment of the N-demethylation and ring hydroxylation of N,N-dimethyl-4-aminoazobenzene (DAB) by rat liver microsomes [17].

Anatomical context of Butter Yellow

• Cytosolic factors that alter the metabolism of N,N-dimethyl-4-aminoazobenzene by rat liver microsomes [18].
• The metabolism of N,N-dimethyl-4-aminoazobenzene (DAB) was investigated in vitro by use of hepatic 10,000g supernatant fraction, microsomes, and purified cytochromes P-450 prepared from rats [19].
• Azoreduction of dimethylaminoazobenzene (DAB) in primary cultures of rat hepatocytes. Effect of hypolipidemic agents [20].
• Human lymphoblast TK6 and mouse C3H10T1/2 cells had the capacity to metabolize dimethylaminoazobenzene and the latter cell line also metabolized benzo[a]pyrene, indicating the presence of constitutive mono-oxygenase activity [21].
• Another resonance dye, p-dimethylaminoazobenzene (DAB) was covalently attached to an antibody directed against human thyroid stimulating hormone (TSH), without loss of antibody activity [22].

Associations of Butter Yellow with other chemical compounds

• The polypeptide is degraded stepwise by using the dimethylaminoazobenzene isothiocyanate/phenyl isothiocyanate double-coupling method, and the released dimethylaminoazobenzenethiohydantoins of amino acids were identified by reversed-phase high-pressure liquid chromatography [23].
• Female Wistar rats were treated sequentially with 4-dimethylaminoazobenzene (4-DAB) and N-nitrosodiethanolamine ( NDEOL ) for periods of 6 weeks [24].
• The F1 hybrids (approximately 50% HBV positive and approximately 50% HBV negative) were treated with a single dose of diethylnitrosamine (NDEA) or p-dimethylaminoazobenzene (DAB) given at 7 days of age, or were untreated [13].
• Cimetidine prevented and reversed delta-aminolevulinate synthetase induction and cytochrome P450 enhancement provoked by p-dimethylaminoazobenzene [15].
• The administration of ASA to DAB treated animals induced Cdk2 (29%) [25].

Gene context of Butter Yellow

• 2. With this aim 5-aminolaevulinate synthetase (ALA-S), microsomal heme-oxygenase (MHO), mitochondrial and cytoplasmic rhodanese activities were examined throughout a period of 35 days in animals exposed to dietary p-dimethylaminoazobenzene (DAB) [26].
• While the detoxifying azoreductase activity was not affected by portal diversion, the activating pathway leading to the binding of 4-dimethylaminoazobenzene metabolites to DNA, a major step for cell carcinogenesis that is mediated by microsomal enzymes, was decreased in shunted rats to about 50 percent of control values [3].
• Both DEN and DAB caused increases in epoxide hydrolase but classical sigmoidal dose-response curves were not obtained [27].
• Isolation and partial purification of mitochondrial and cytosolic rhodanese from liver of normal and p-dimethylaminoazobenzene treated mice [28].
• This drug did not modify either increased lipid peroxidation or diminution of the natural antioxidant defence system (inferred by catalase activity) induced by p-dimethylaminoazobenzene [15].

Analytical, diagnostic and therapeutic context of Butter Yellow

• Structures of antithrombin III Basel and normal antithrombin III isolated from the same patient were compared by peptide mapping using the dimethylaminoazobenzene isothiocyanate precolumn derivatization technique [29].
• Isolation and HPLC of N-epsilon-lithocholyl lysine as its fluorescamine and dimethylaminoazobenzene isothiocyanate derivatives [30].
• Different methods of sequence analysis complemented each other, mainly the manual dimethylaminoazobenzene isothiocyanate method and and the use of liquid-phase sequencer degradations [31].
• The resultant conjugate was used in a sandwich immunoassay for TSH antigen: silver surfaces coated with anti-TSH antibody captured TSH antigen which in turn captured the DAB-anti-TSH antibody conjugate [22].
• Survival times were decreased by R and chemotherapy due to combined toxicities of DAB and treatments and were partially restored by MTP [32].

References