Disease relevance of N-NITROSODI-N-BUTYLAMINE

• Suppression of dibutylnitrosamine-induced bladder carcinomas in hamsters by dietary indole [1].
• Mice receiving DBN precursors showed a delayed gain in body weight as well as decreased protein level and 5-nucleotidase activity [2].
• Activation of N-ras gene in a rat hepatocellular carcinoma induced by dibutylnitrosamine and butylated hydroxytoluene [3].
• Meanwhile, incidence of bladder papillomas was only 20% in mice receiving VF in addition to DBN precursors, and bladder papillomas were completely absent in mice receiving bran in addition to DBN precursors [2].
• Piperonyl butoxide, dibutylnitrosamine and nitrososarcosine had no effect on the acute toxicity of DMN [4].

High impact information on N-NITROSODI-N-BUTYLAMINE

• Effect of dietary indole on the urinary bladder tumorigenesis by chronic dibutylnitrosamine (DBN) treatment was evaluated in hamsters [1].
• Male F344 rats were given 0.05% N,N-dibutylnitrosamine in their drinking water for 4 wk and then treated with basal diet containing 2% butylated hydroxyanisole (BHA), 1% butylated hydroxytoluene (BHT) with 7 ppm vitamin K, 0.8% ethoxyquin, 5% sodium L-ascorbate, 5% sodium erythorbate, or no added chemical for 32 wk [5].
• Promoting activities of sodium phenobarbital (PB) and sodium saccharin (SS), incorporated in a semisynthetic diet (AIN-76A), on 2-stage carcinogenesis initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) or N,N-dibutylnitrosamine (DBN) in male F344 rats were investigated [6].
• With microsomes from PB-pretreated rats, inhibition by mAb-2B1 indicated a 62% contribution by cytochrome P450 2B1 to debutylation of NDBA and 65% to depropylation of NDPA [7].
• The involvement of cytochrome P450 in the cytotoxicity and DNA damage-repair induced by N-nitrosodipropylamine (NDPA), N-nitroso-n-butyl-n-propylamine (NBPA), and N-nitrosodibutylamine (NDBA) was investigated in cultured hepatocytes isolated from untreated, phenobarbital (PB)- and pyridine (PYR)-pretreated rats [8].

Chemical compound and disease context of N-NITROSODI-N-BUTYLAMINE

• N-Propyl-N-butylnitrosamine and DBN induced hepatomas, but simultaneous development of esophageal tumors were observed only with the former [9].

Biological context of N-NITROSODI-N-BUTYLAMINE

• Tissue, species, and substrate concentration differences in the position-selective hydroxylation of N-nitrosodibutylamine. Relationship to the distribution of cytochrome P-450 isozymes 2 (IIB) and 5 (IVB) [10].
• Revertants induced by all the nitrosamines except diethylnitrosamine and dibutylnitrosamine resulted mainly from damage to G-C base pairs in TA104 [11].
• The carcinogen dibutylnitrosamine (DBN), given subcutaneously in repeated doses causes a loss of polyploidy prior to cancer development [12].
• The effect of 13-cis-retinoic acid on cell proliferation in normal urothelium and during early stages in N-nitrosodibutylamine (DBN) induced malignant transformation was studied in male hairless mice [13].
• Whole-body autoradiography with 14C-labelled N-nitrosodibutylamine (NDBA) in pregnant Syrian golden hamsters on day 15 of gestation showed an uptake of radioactivity in the fetuses and a localization of metabolites in the tracheobronchial and nasal mucosa [14].

Anatomical context of N-NITROSODI-N-BUTYLAMINE

• Microsomes from BHT-pretreated rats showed a slight increase in activity for N-dealkylation of NDBA and BNPA [7].
• In vitro metabolism of N-nitrosodibutylamine (NDBA) and of three fluorinated analogs, N-nitroso-4,4,4-trifluorobutyl-butylamine (NDBA-F3), N-nitroso-bis(4,4,4-trifluorobutyl)-amine (NDBA-F6) AND N-nitroso-bis(2,2,3,3,4,4,4-hepafluorobutyl)amine (NDBA-F14) was investigated with rat liver microsomes [15].
• The structure of the glycocalyx was not affected by 12 weeks of treatment with dibutylnitrosamine, a known bladder carcinogen [16].
• The effect of 13-cis-retinoic acid on dibutylnitrosamine induced polyploidy changes in mouse urothelium [12].
• Rubber nipples and pacifiers were analysed for volatile N-nitrosamines using gas chromatography-thermal energy analysis after extraction with 'artificial saliva'. All of the 17 samples tested were found to contain at least two of the following: N-nitrosodimethylamine, N-nitrosodiethylamine, N-nitrosodibutylamine and N-nitrosopiperidine [17].

Associations of N-NITROSODI-N-BUTYLAMINE with other chemical compounds

• The goal of this work was to study the effect of the most common Egyptian food items, Vicia faba beans (VF) and bran, on the carcinogenicity of dibutylnitrosamine (DBN) precursors (dibutylamine and nitrite) [2].
• At the highest concentration tested, butylated hydroxyanisole significantly inhibited the in vitro formation of N-nitrosodi-n-butylamine from dibutylamine and nitrite by 35% [18].
• The activity of glutathione S-transferase activity was inhibited after treatment of the male mice with diphenylnitrosamine (-60%), dibutylnitrosamine (-60%), and methylpropylnitrosamine (-81%), while, ethylmethylnitrosamine and ethylbutylnitrosamine had no effect on such activity [19].
• Significant correlations between mean intragastric pH values and mean N-nitrosodi-n-butylamine level (P = 0.005) and total volatile N-nitrosamine contents (P = 0.009) were observed [20].
• Effect of butylated hydroxyanisole added in vitro or administered to rats on N,N-dibutylnitrosamine and N-butyl-N-(4-hydroxybutyl)nitrosamine metabolism by post-mitochondrial supernatant of liver homogenates [21].

Gene context of N-NITROSODI-N-BUTYLAMINE

• The four-fold increase in mutagenicity in the presence of cytochrome b(5) was consistent with increasing alkyl chain length up to dibutylnitrosamine, which was poorly activated by CYP2E1 [22].
• Alkaline phosphatase was also elevated when bran was administered with DBN precursors [2].
• Cytochrome b5 content was increased by 190% of the control value in mice treated with N-nitrosomethylbutylamine, while N-nitrosodibutylamine induced the lowest increase (+20%) [23].
• Swiss albino mice showed an enhanced expression of an approximately 58 kDa glycoprotein in liver cells upon exposure to a potential hepatocarcinogen N-nitrosodibutylamine (DBN) [24].

Analytical, diagnostic and therapeutic context of N-NITROSODI-N-BUTYLAMINE

• The initial effect of a single subcutaneous injection of 0.01 ml of dibutylnitrosamine on the mouse (hr/hr strain) urinary bladder epithelium was a block in DNA synthesis in the diploid cells followed by a regenerative reaction [25].
• In our animal experiments we used a chemical agent (dibutylnitrosamine) to induce urinary bladder tumor in rats, then this was implanted under the dorsal skin of rats of the same strain to gain a standard tumor preparation [26].
• Cystoscopy of chemically induced bladder neoplasms in rabbits administered the carcinogen dibutylnitrosamine [27].

References