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PubMed1980

Transnitrosation by nitrosamines and nitrosoureas.

The factors that determine alicyclic nitrosamines can act as transnitrosating agents include steric and electronic factors, as well as factors relating to the basicity of the parent amine. The slower transnitrosating agents, such as nitrosopipecolic acid, can nitrosate piperidine at pH 1.7, while the nitrosopiperazines cannot. Nitrosoureas, particularly nitrosotrialkylureas, are rapid transnitrosating agents and all are capable of nitrosating piperidine to high yields, even at pH 3.6.

Chemical Phenomena↗
PubMed1980

Kinetics of nitrosamine formation in mice following oral administration of trace-level precursors.

Groups of 3-5 Swiss CD1 mice were gavaged with aqueous solutions of sodium nitrite (250 micrograms), followed immediately by morpholine (5 micrograms) or dimethylamine (250 micrograms). At subsequent intervals, up to 30-60 min, mice were frozen, pulverized in liquid nitrogen and extracted with methylene chloride. Volatile nitrosamines were then quantitatively determined using a Thermal Energy Analyzer, interfaced to GC or HPLC. Biosynthesis of both N-nitrosodimethylamine (NDMA) and N-nitrosomorpholine (NMOR) showed a time-dependent increase for 3 and 9 min, respectively, followed by a steady decline. Levels of NDMA and NMOR were generally less than 0.1 ng/g in control mice gavaged with amine or nitrite alone. Zero-time recovery of NDMA and NMOR ranged from 50-70% and 70-90%, respectively. Biosynthesis of NDMA and NMOR was inhibited by prior administration of ascorbic acid, sodium ascorbate or ammonium sulfamate.

Administration, Oral↗
PubMed1980

Combination of a GC-TEA and a GC-MS-data system for the microgram/kg estimation and confirmation of volatile N-nitrosamines in foods.

An analytical procedure has been outlined in which volatile N-nitrosamines in foods are isolated by vacuum distillation, cleaned up, identified and quantified by GC-TEA and qualitatively confirmed by GC-MS, coupled with a data system. Spectra are presented which demonstrate that this technique is capable of confirming NDMA and NPYR in a variety of foods at levels of 1 to 10 micrograms/kg. Unequivocal confirmation is based on three types of evidence: (1) the compound is TEA positive; (2) the compound has the correct retention time on a packed and on a capillary column; (3) the complete mass spectrum closely matches standard spectra. These procedures have been used to confirm the presence of trace levels of NDMA in domestic beer and in non-fat dry milk.

Chromatography, Gas↗
PubMed1980

Further studies on the occurrence of volatile and non-volatile nitrosamines in foods.

Approximately 250 samples of various foods, such as cured meat products, fried bacon, cooked-out bacon fats, baby foods containing meats, tomato products, cooked pizza, powdered and evaporated milk, mushrooms and different varieties of alcoholic beverages, were analysed by GLC-TEA for the presence of volatile nitrosamines. The levels detected in cured meat products (both cooked and uncooked) were very low, and both their incidence (at greater than 1 microgram/kg) and concentrations were much lower than those observed in a 1974 survey. The levels of N-nitrosopyrrolidine (NPYR) in fried bacon and cooked-out bacon fats were also somewhat lower than those observed at the end of 1976, but the decrease may not be significant. Traces (mean, 1.5 micrograms/kg) of N-nitrosodimethylamine (NDMA) were detected in 21 of 22 samples of beers and ales. Most of the remaining foods gave negative results, excepting the skim milk powders, which contained minute traces (mean, 0.4 micrograms/kg) of NDMA. An HPLC-TEA method was developed for the analysis of N-nitrosoproline (NPRO) and N-nitrososarcosine (NSAR) in raw and fried bacon. A study of the heat-induced decarboxylation of these nitrosamino acids suggests that these compounds are heat-labile and would not be expected to occur in fried foods at significant levels. Their presence, however, may lead to the formation of traces of NPYR and NDMA during frying at lower temperatures.

Beverages↗
PubMed1980

Nitrosamines in new automobiles.

The volatile nitrosamines, N-nitrosodimethylamine (NDMA), N-nitrosomorpholine (NMOR), N-nitrosodiethylamine (NDEA) and possibly N-nitrosodibutylamine (NDBA) have been found to be present as airborne pollutants in the interiors of new (1979 model) automobiles. In the 38 automobiles tested, the levels ranged from 0.07 to 0.83 micrograms/m3 (average 0.3 micrograms/m3) for NDMA, from 0.07 to 2.5 micrograms/m3 (average 0.67 micrograms/m3) for NMOR, from 0.04 to 0.39 micrograms/m3 (average 0.11 micrograms/m3) for NDEA and trace levels (less than 0.01 micrograms/m3) for NDMA.

Air Pollutants↗
PubMed1980

[Effect of various blockers of nitrite and nitrogen oxide on the formation of nitrosamines].

The effects of galacturonic, gallic, acetylneuraminic acid, ascorbate, cysteine, glutathion and imidazole on the formation of dimethylnitrosamine and diethylnitrosamine was studied in a simple aqueous medium with four different nitrite contents (50, 100, 500 and 1 000 ppm) and the two amines, compared with control samples. The nitrosamines were determined by the TELLING method (confirmed by photolysis). The results observed were compared with the laws of fixing nitrite in the form of nitrogen oxide, studied previously. For sarcosin and imidazole, the fixing takes into account the phenomena observed. The other substances lead to a conclusion that there are two stages in the process: 1) fixing of the nitrite to a greater or lesser degree in the form of a nitrogen oxide complex, 2) direct effect on the nitrosation reaction which is catalysed or slowed down. The discussion based on the literature, concludes that the final nitrosation reaction give rise to free radicals, even in an aqueous medium.

Antioxidants↗
PubMed1980

[Analysis of volatile nitrosamines in foods and beverages: validity of results].

Analytical methods for volatile nitrosamines in foods and beverages are described. The possibilities of loss and formation of these compounds are discussed for each analytical step. The validity of the gas chromatographic and high performance liquid chromatographic determinations is evaluated for each detector type.

Beverages↗
PubMed1981

Gastritis, nitrosamines, and gastric cancer.

Gastritis is associated with peptic ulcer, gastroenterostomy, pernicious anemia, and exposure to nitrosamines. Once established, the process may be self-perpetuating, resulting in atrophy, metaplasia, dysplasia, and neoplasia. This can be explained by the process of endogenous nitrosation of amines in the inflamed gastric mucosa. Evidence is presented to support this hypothesis. Several drugs given parenterally have been identified as mutagenic nitroso compounds in homogenates of human and canine antral mucosa. Nitrite for this process is apparently derived from the inflamed mucosa. Different amines appear to be nitrosated at different places in the antrum, suggesting the presence of site-specific enzymes that control these reactions.

Animals↗
PubMed1980

Comparison of the carcinogenic effects of five nitrosamines in guinea pigs.

Five nitrosamines which were potent carcinogens in rats or hamsters were administered by gavage in olive oil solution twice a week to 20 male strain 2 guinea pigs. Nitroso-2,6-dimethylmorpholine given at 80 mg/kg/week for 12 weeks or at 32 mg/kg/week for 35 weeks gave rise to hemangioendothelial sarcomas of the liver in 6 and 19 animals, respectively. The same tumors were induced in 18 animals by dinitroso-2,6,dimethylpiperazine, together with hepatocellular carcinomas in six animals. Nitrosomethyldodecylamine also induced mainly hemangioendothelial sarcomas of the liver (12 animals). A few bile duct carcinomas were also observed. Neither nitrosoheptamethyleneimine nor nitrosomethyldiethylurea seemed to induce tumors in guinea pigs under our conditions.

Animals↗
PubMed1980

Effect of simultaneous administration of leupeptin on induction of bladder tumors in rats by N-butyl-N-(4-hydroxybutyl)-nitrosamine.

Male Wistar rats were given a diet containing 0.1% leupeptin, a microbial protease inhibitor, and drinking water containing 0.01% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) for 8 weeks. Leupeptin did not have any detectable effect on the induction of bladder tumors by BBN in week 40, in terms of the weight of the bladder including the tumor, the number of tumors per bladder, the extent of invasion, or the incidences of hyperplasia, papilloma, and cancer. This result is in marked contrast to the previous findings that leupeptin enhanced BBN-induced bladder carcinogenesis when administered continuously after BBN-treatment.

Animals↗
PubMed1980

Interaction of the tobacco-specific nitrosamines, methylethylnitrosamine and N-nitrosonornicotine, with DNA and guanosine.

In vitro binding of the tobacco-specific nitrosamines, methylethylnitrosamine (MEN) and nitrosonornicotine (NNN), to exogenous DNA and guanosine was studies in a rat liver microsome-catalyzed system. MEN (N-[ethyl-1-14C]) binds covalently to calf thymus DNA whereas NNN (N'-[pyrrolidine-2-14C]) binds only to guanosine but not to DNA. Pretreatment of the rats with either phenobarbital (PB) or 3-methylcholanthrene (MC) greatly diminishes the binding of 14C-MEN to DNA. Both MEN-demethylase and -deethylase activities are stimulated by PB pretreatment and inhibited by MC pretreatment, but the degree of stimulation and inhibition of the two dealkylases are not the same. Addition of cytosol to the incubation system does not enhance but suppresses the binding of 14C-MEN to DNA. Inclusion of mitochondria in the system has no effect on the binding. Addition of benzylamine (250 microM), which is a potent inhibitor of dimethylnitrosamine-demethylase, however totally abolishes the binding of 14C-MEN catalyzed by microsomes. The data suggest that ethylcarbonium ion may be the metabolically activated intermediate of MEN that binds to DNA.

Animals↗
PubMed1980

Inhibitory effect of an aromatic retinoic acid analog on urinary bladder carcinogenesis in rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine.

The inhibitory effect of an aromatic retinoic acid analog, ethyl all-trans-9-(4-methoxy-2,3,6-trimethylphenyl)-3,7-dimethyl-2,4,6,8-nonatetraenoate, on bladder carcinogenesis in rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) was evaluated. Administration of 50 ppm of aromatic retinoid in the diet before BBN in the drinking water reduced the incidence of papillary or nodular hyperplasia as a preneoplastic lesion of the bladder epithelium (P < 0.05). When given before, during or after BBN, it also greatly reduced the incidence of papilloma (P < 0.001 before BBN, P < 0.01 during or after BBN treatment), and slightly inhibited the development of cancer. Administration of 100 ppm of aromatic retinoid before or during BBN administration also reduced the incidences of papillary or nodular hyperplasia (P < 0.01 before BBN, P < 0.05 during BBN treatment), and its administration before, during or after BBN treatment greatly reduced the incidences of papilloma (P < 0.001), and cancer (P < 0.01 before or after BBN, P < 0.001 during BBN treatment). Similar results were obtained by assessing the effect of the retinoid on the average numbers of various epithelial lesions per 10 cm length of basement membrane of the bladder in tissue slices. These results show that the aromatic retinoid inhibits both the initiation and promotion of bladder carcinogenesis induced in rats by BBN, and that its effect is dose-dependent.

Animals↗
PubMed1980

Inhibition by an aromatic retinoid of DNA damage induced by the bladder carcinogen N-butyl-N-(3-carboxypropyl)nitrosamine.

The reversible inhibitory action of an aromatic analog of retinoic acid, ethyl all-trans-9-(4-methoxy-2,3,6-trimethylphenyl)-3,7-dimethyl-2,4,6,8-nonatetraenoate (aromatic retinoid) on bladder carcinogenesis was studied by biochemical and histopathological methods. fischer 344 female rats were fed a diet containing the aromatic retinoid (0, 12.5 or 50 ppm) for 56 days. On day 57, 60 or 70, 50 mg/kg body weight of N-butyl-N-(3-carboxypropyl)nitrosamine (BCPN) in a volume of 0.3 ml was directly instilled intravesically through a urethral catheter. DNA damage in rat bladder epithelial cells 2, 24 and 48 hr after administration of BCPN was examined by measuring the change in sedimentation profile of the DNA in 5 approximately 20% alkaline sucrose gradients. DNA sedimentation was measured by a fluorometric procedure. Histopathological examination of the bladder epithelium was performed at the same time. Two hours after a 5-min exposure to BCPN, DNA damage at the urothelium was observed in rats fed the diet without the aromatic retinoid, but the damage was repaired after 24 and 48 hr. The highest dose of the aromatic retinoid almost completey prevented DNA damage by BCPN on days 57 and 60. A lower dose of the aromatic retinoid did not prevent DNA damage by BCPN on days 57, 60, and 70, while the higher dose did not prevent damage by BCPN on day 70. No histological changes were observed in the urothelium of rats treated with the aromatic retinoid and BCPN, and electron microscopy showed that the epithelium also remained normal. DNA damage was induced by BCPN at the urothelium, and the damage was inhibited by previous administration of the aromatic retinoid.

Animals↗
PubMed1981

N-butyl-N-(4-hydroxybutyl)nitrosamine-induced urinary bladder cancer in C57BL/6 X DBA/2 F1 mice as a useful model for study of chemoprevention of cancer with retinoids.

Highly invasive carcinomas of the urinary bladder were induced in male C57BL/6 X DBA/2 F1 (hereafter called B6D2F1) mice by gastric intubation of N-butyl-(4-hydroxybutyl)nitrosamine (OH-BBN) using a quantitative dosing schedule. Animals received either 5 or 10 mg OH-BBN per intubation, two times each week, for 9 weeks for a total dose of either 90 or 180 mg, and they were killed 6 months after the first carcinogen intubation. Seven days after the final intubation of OH-BBN, animals were fed either a placebo diet or diet supplemented with either 150 or 200 mg 13-cis-retinoic acid per kg of diet. A 41 and 43% incidence of urinary bladder cancer was observed in mice given the low and high dose of carcinogen, respectively, and fed a placebo diet. Sixty-seven % of the carcinomas induced in these animals invaded either into or through the urinary bladder wall. Varying degrees of transitional and either squamous or glandular or both squamous and glandular differentiation were observed in the carcinomas. Feeding of diet supplemented with 13-cis-retinoic acid reduced cancer incidence; the degree of reduction was proportional to the dose of retinoid administered. The highly invasive nature of the carcinomas induced by quantitative administration of OH-BBN in B6D2F1, mice provides a useful animal model of the highly invasive variant of human transitional cell urinary bladder cancer in which to study chemoprevention by retinoids as well as other compounds.

Animals↗
PubMed1978

Effect of vitamin A acetate on urinary bladder carcinogenesis induced by N-butyl-N-(4-hydroxybutyl)nitrosamine in rats.

The effect of vitamin A acetate on the urinary bladder carcinogenicity of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) was determined in male Wistar rats. Vitamin A acetate at the dose administered induced no changes in the urinary bladder or other organs when administered without the carcinogen. However, hypervitaminosis A inhibited keratinization and squamous metaplasia in bladder lesions induced by BBN, and the incidence of transitional cell carcinoma and papilloma of the urinary bladder was significantly reduced at a dose greater than 100 IU/g diet (P less than 0.02). The present experiment suggests that for the urinary bladder epithelium of rats hypervitaminosis A reduced susceptibility to the tumorigenicity of BBN.

Animals↗
PubMed1976

Mutagenicity of cyclic nitrosamines in Escherichia coli following activation with rat liver microsomes.

Ten cyclic nitrosamines were tested for mutagenicity in Escherichia coli after incubation in vitro with 9000 X g microsomal supernatants prepared from rat liver, and the results were compared with carcinogenicity data from the same species. None of the compounds was mutagenic in the absence of microsomes. Seven carcinogenic compounds, nitrosopyrrolidine, nitrosopiperidine, nitrosohexamethyleneimine, nitrosoheptamethyleneimine, nitrosomorpholine, dinitrosopiperazine, and dinitrosohomopiperzine, were mutagenic after microsomal activation. One compound, nitrosohepamethyleneimine, was toxic to the bacteria. Two noncarcinogens, 1-nitrosopiperazine and 1-methyl-4-nitrosopiperazine, and 1 strong carcinogen, 2,6-dimethyldinitrosopiperazine, were not mutagenic with or without microsomal incubation. The liver microsome preparation activated equally well those compounds that are liver carcinogens in Sprague-Dawley rats, and compounds for which the liver is not a target organ.

Animals↗
PubMed1993

Tumor induction in mice administered neonatally with N-bis(2-hydroxypropyl)nitrosamine (BHPN).

Two subcutaneous injections of N-bis(2-hydroxypropyl)nitrosamine (BHPN) to mice on day 1 and 8 induced tumors of the lung, liver, nasopharynx and pancreas, when animals were killed at the end of one year. The tumor incidences of lung were 90-100%; those of liver 60-92%; those of nasopharynx 3-13%; those of pancreas 2-3%, respectively. The average tumor nodules of lung and those of liver increased in a dose-dependent manner. Two doses of 50 mg/g body weight of BHPN induced one duct cell carcinoma and one acinar cell adenoma of pancreas in a mouse, respectively.

Animals↗
PubMed1993

[Carcinogenic N-nitrosamines in the tire industry].

The level of volatile carcinogenic N-nitrosamines (NA) was studied in the air of various technological sites of tyre production. Reported total levels of NA in air exceeded MACs set in certain countries for the same enterprises. For example, German total MAC for 12 carcinogenic NA is 1 g/m3. N-nitrosomorpholine appeared to have the highest level (91 g/m3), probably, because its derivatives are used as raw material for technological process. Relative rate of volatile NA release from rubber samples containing 4-nitrosodiphenylamine (modifier) was studied. The parameter was reported to have no influence on NA outlet in conditions simulating technological process. NA was detected by means of gas chromatography with thermal energy detector TEA 502A provided by Thermo Electron Corporation, USA. The article necessitates regulation of NA in tyre production and better rubber mixtures to control the pollution of atmosphere.

Air Pollutants, Occupational↗