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PubMed2004

Determination of volatile N-nitrosamines in irradiated fermented sausage by gas chromatography coupled to a thermal energy analyzer.

Volatile N-nitrosodimethylamine (NDMA) and N-nitrosopyrrolidine (NPYR) in irradiated pepperoni and salami sausages were determined using a gas chromatography coupled to a thermal energy analyzer (GC-TEA). These fermented sausages with aerobic or vacuum packaging were irradiated at 0, 5, 10, and 20 kGy, and then stored for 4 weeks at 4 degrees C. Both NDMA and NPYR in the fermented sausage were significantly reduced by irradiation. The vacuum packaging showed significantly lower (P < 0.05) N-nitrosamine levels than that of the aerobic ones. After storage, the contents of NDMA and NPYR in the irradiated sausage were lower than those of the non-irradiated control. Results indicated that a high dose of irradiation (>10 kGy) was needed to reduce the carcinogenic N-nitrosamines in the fermented sausage during storage and the GC-TEA analysis was effective in determining the N-nitrosamines in irradiated meats even at low trace levels.

Chromatography, Gas↗
PubMed2004

Rabbit liver microsomal system: study of interaction with two model N-nitrosamines and their metabolism.

Rabbit liver microsomes of control (non-treated) or animals induced either by ethanol (EtOH) or phenobarbital (PB) were incubated with N-nitrosodimethylamine (NDMA) or N-nitrosomethylaniline (NMA). Difference spectroscopy showed that NMA is bound to the substrate-binding site of cytochrome P-450 (CYP) isoforms as heme ligand in control and EtOH pre-treated microsomes. On the other hand, PB-induced microsomes exhibit with NMA substrate type of spectra. NDMA does not provide any type of binding spectra with used microsomal systems. Oxidative bio-activation of N-nitrosamines by the microsomal CYP isoforms was measured as formaldehyde formation. Analysis of reaction kinetics in control microsomes revealed, for both substrates, two values of Michaelis-Menten constant (K(m)) for, K(m) values of 0.03 and 0.13 mmol/l for NDMA, and 0.30 and 0.82 mmol/l for NMA. Induction of animals with EtOH resulted in a decrease in the K(m) value for both substrates. In contrast, PB treatment caused an elevation of K(m) value for NDMA. Based on these data, we conclude that EtOH-inducible microsomal CYP isoforms (mainly CYP2E1) are responsible for binding and N-demethylation metabolism of both studied N-nitrosamines in rabbit liver microsomal system. The role of the other CYP isoforms involved in the metabolism of mentioned N-nitrosamines is discussed.

Animals↗
PubMed1991

Epstein-Barr virus activators, mutagens and volatile nitrosamines in preserved food samples from high-risk areas for nasopharyngeal carcinoma.

Representative samples of preserved foods collected from high-risk areas for nasopharyngeal carcinoma were assayed for capacity to induce Epstein-Barr virus (EBV) by measuring induction of the DR promoter gene or of genes for early antigens in Raji cells. The two assays gave concordant results, but the DR induction assay detected EBV-inducing substances at lower concentrations and more reproducibly. Three of 17 preserved food items were active in both assays; they were also weakly mutagenic in the SOS chromotest and contained low or moderate levels of volatile N-nitrosamines. After in-vitro nitrosation, the levels of mutagens and nitrosamines increased, whereas EBV-inducing activity was unchanged or decreased. Thus, EBV inducers appear to be a different class of substances from mutagens and volatile N-nitrosamines but could act with them in the etiology of nasopharyngeal carcinoma.

Food Analysis↗
PubMed1991

Relevance of N-nitrosamines to oesophageal cancer in China.

Oesophageal cancer occurs at a very high frequency in certain areas of China, especially in Linxian county, Henan province. Previous studies suggested that N-nitroso compounds play a causative role. In order to study further the exposure of Linxian inhabitants, the intake of N-nitrosamines in the diet was determined. The total daily intake of volatile nitrosamines and of N-nitroso-N-methylbenzylamine (NMBzA) was higher in Linxian than in two other counties. NMBzA can induce cancer in animal and human oesophageal epithelium. Human fetal oesophageal epithelia were cultured with NMBzA for 4 h, and eight monkeys were treated with NMBzA. High-molecular-weight DNA extracted from explants and from the oesophageal epithelia of monkeys induced malignant transformation of NIH 3T3 cells. Alu and monkey-specific repeat sequences were present in transformed cells, and H-ras was found in the transforming DNA. Human fetal oesophageal epithelium cultured with NMBzA was transplanted into the mesentery of BALB/c nude mice. Tumours were found after eight months; and the Alu sequence was present in DNA extracted from tumours induced by NMBzA, showing that the tumours were of human origin. The results provide direct evidence that NMBzA is carcinogenic in human oesophageal epithelium and that N-nitrosamines are one of the causative factors of oesophageal cancer in Linxian county.

Animals↗
PubMed1991

Occurrence of and exposure to N-nitrosamines in Sweden: a review.

During the last ten years, over 900 samples of foods, snuff and other products on the Swedish market were analysed for N-nitrosamines. The average daily intake of volatile N-nitrosamines from foods was estimated to be 0.29 micrograms/person, and the daily intake of tobacco-specific N-nitrosamines from snuff was calculated to be up to 110 micrograms/snuff user.

Food Analysis↗
PubMed1976

[Formation of nitrosamines in the digestive tract].

Nitrosamines are carcinogenic compounds synthetized from amines and nitrites or nitrates, if nitrates in the reaction medium may be reduced to nitrites. Nitrosation is determined in the digestive tract of several species of laboratory animals. Two physiochemical factors appear to determine in vitro nitrosamine formation: the type of amine and the medium pH. The property of secondary amines to nitrosate is inversely related to amine basicity (checked in vivo), and it increases with the medium acidity. In vitro studies show that different types of bacteria can, even at neutral pH, catalyze nitroamine formation from their precursors. However, the role of digestive tract microbial flora in nitrosamine synthesis in the gut cannot be affirmed due to lack of in vivo studies.

Amines↗
PubMed1979

Metabolism of three radiolabeled pancreatic carcinogenic nitrosamines in hamsters and rats.

The in vivo metabolism and disposition of three radiolabeled N-nitrosamines which are carcinogenic for the pancreas of the hamster but not the rat have been examined. N-[1-14C]Nitrosobis(2-oxopropyl)amine (BOP), N-[1-14C]nitrosobis(2-hydroxypropyl)amine (BHP), and their suggested proximate pancreatic carcinogenic metabolite N-[1-14C]nitroso-(2-hydroxypropyl)(2-oxopropyl)amine (HPOP) were metabolized and exhaled as 14CO2 to various extents somewhat proportional to their carcinogenic potency. More than 50% of the dose of BOP and HPOP was exhaled as 14CO2, whereas 26% of BHP was excreted this way, and 40% of BHP was excreted unchanged in the urine. Administered BOP was excreted to a small extent in the urine of both species as HPOP and BHP. No other nitrosamine metabolites were detected in urine. HPOP and BHP were detected in the pancreatic juice and bile of both species after administration of BOP and BHP. The results suggest that pancreatic ductular carcinogenesis in the hamster as a result of exposure to BOP is not due to secretion of carcinogenic metabolities in the pancreatic juice or reflux of bile containing nitrosamine metabolites into the ducts. Carcinogen metabolic activation appears to be by an oxidative pathway.

Animals↗
PubMed1990

Mass spectrometric analysis of tobacco-specific nitrosamine hemoglobin adducts in snuff dippers, smokers, and nonsmokers.

Hemoglobin adducts of the carcinogenic tobacco-specific nitrosamines 4-(methylnitrosamino)-1(3-pyridyl)-1-butanone and N'-nitrosonornicotine were quantified in blood samples collected from snuff dippers, smokers, and nonsmokers. Mild base treatment of hemoglobin adducted by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone or N'-nitrosonornicotine releases 4-hydroxy-1-(3-pyridyl)-1-butanone (HPB). HPB was enriched by solvent partitioning and derivatized to its pentafluorobenzoate. After purification by high performance liquid chromatography, HPB-pentafluorobenzoate was analyzed by capillary column gas chromatography with detection by negative ion chemical ionization mass spectrometry and selected ion monitoring. [4,4-D2]HPB was used as internal standard. The detection limit for HPB-pentafluorobenzoate was approximately 100 amol/injection or 5 fmol/g hemoglobin. Mean adduct levels (fmol HPB/g hemoglobin) were 517 +/- 538 (SD) in snuff dippers, 79.6 +/- 189 in smokers, and 29.3 +/- 25.9 in nonsmokers. Adduct levels in snuff dippers and in a subgroup of smokers were higher than would have been predicted solely based on estimates of exposure to tobacco-specific nitrosamines. The results of this study provide the first measurements of tobacco-specific nitrosamine hemoglobin adducts in humans and suggest new approaches to understanding the metabolic activation of 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone and N'-nitrosonornicotine in humans.

Adult↗
PubMed1989

[Investigation on nitrosamine in drinking water in Huang Shi--a high-risk area of stomach cancer in Fujian province].

Huang Shi town in Fujian province is one of the high-risk area of stomach cancer in China with a standard mortality rate of 61.19/100,000 in males. Epidemiologic survey showed that it was related to the severe contamination of Mu-Lan river system by which the drinking water for the residents was provided. Thirty-three water samples in the summer and winter times, filtrated and unfiltrated, from different spots along this river system were collected. The concentrations of nitrite and nitrosamine were determined. NDMA, NDEA, NDPA, NDBA, NPIP and NMOR by GC-TEA and three unknown peaks preliminarily identified as non-volatile nitrosamine by LC-TEA could be detected in these samples. The kinds and the content of nitrosamine in the samples collected in the winter time were all significantly higher than those collected in the summer, P values were all less than 0.01. Its possible significance in the causes of gastrointestinal tumors is discussed.

China↗
PubMed1988

Alterations in pancreatic islet function produced by carcinogenic nitrosamines in the Syrian hamster.

Exposure of hamsters to 5 daily doses of 20 mg/kg N-nitrosobis(2-oxopropyl)amine (BOP) or 76 mg/kg N-nitroso(2-hydroxypropyl)(2-oxopropyl)amine (HPOP), resulted in reduced insulin secretion in freshly isolated pancreatic islets. These treatments also reduced plasma insulin and glucose levels, and were hepatotoxic. The inhibition of insulin secretion, however, was transient. Islets isolated from treated hamsters that were then placed in culture secreted elevated levels of insulin for many months. When cultured islets were directly exposed to the nitrosamines for 3 days, there was also a transient reduction of insulin secretion that was subsequently normalized after removal of the nitrosamine from the medium. These results show that BOP and HPOP modify beta-cell function both directly, and possibly indirectly, via damage to the liver. Furthermore, the lack of immediate inhibition of insulin secretion when islets were incubated in the presence of BOP or HPOP as well as glucose, suggests that the nitrosamines do not bind to the glucose receptor.

Animals↗
PubMed1988

Induction of lung and exocrine pancreas tumors in F344 rats by tobacco-specific and Areca-derived N-nitrosamines.

The tobacco-specific N-nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), as well as the Areca-derived N-nitrosoguvacoline (NG) were assayed for carcinogenicity in male F344 rats by lifetime administration in the drinking water. Groups of 30 to 80 rats were treated with 0.5 ppm, 1.0 ppm, or 5.0 ppm of NNK; 5.0 ppm of NNAL, 20 ppm of NG, a mixture of 20 ppm of NG and 1 ppm of NNK, and water only in the control group. The approximate total doses of the nitrosamines (mmol/kg of body weight) in these groups were: NNK, 0.073, 0.17, and 0.68; NNAL, 0.69; NG, 4.1; NG and NNK, 4.1 and 0.17. As in previous assays in which NNK was tested by s.c. injection, the lung was its principle target organ. Lung tumor incidences in the 0.5-, 1.0-, and 5.0-ppm groups were nine of 80, 20 of 80, and 27 of 30 compared to six of 80 in the control rats. This trend was significant, P less than 0.005. Significant incidences of nasal cavity and liver tumors were observed only in the rats treated with 5.0 ppm of NNK. In contrast to the results of the s.c. bioassays of NNK, tumors of the exocrine pancreas were observed in five of 80 and nine of 80 rats treated with 0.5 and 1.0 ppm. This trend was significant, P less than 0.025. This is the first example of pancreatic tumor induction by a constituent of tobacco smoke. It is also the first finding of duct-like carcinomas in the rat pancreas, including one tumor containing epidermoid, keratin-generating tissue. NNAL, the major metabolite of NNK, induced lung tumors in 26 of 30 rats and pancreatic tumors in eight of 30 rats. It appears to be the proximate pancreatic carcinogen of NNK. NG induced pancreatic tumors in four of 30 rats, P less than 0.05. This finding requires confirmation. The mixture of NG and NNK induced lung tumors in eleven of 30 rats. There were no apparent synergistic interactions of NG and NNK. The observation of benign and malignant tumors of the lung and pancreas of rats treated with the tobacco-specific nitrosamines NNK and NNAL is discussed in respect to the causal association between cigarette smoking and cancer of the lung and pancreas.

Animals↗
PubMed1977

Microsome-mediated mutagenesis in V79 Chinese hamster cells by various nitrosamines.

A microsome-mediated mutagenesis system has been established with the V79 Chinese hamster cell line. The cells, grown in monolayer, were treated with various nitrosamines in the presence of a postmitochondrial fraction ((S15) from rat liver and a reduced nicotinamide adenine dinucleotide-generating system for 1 hr, washed and incubated for 2 to 3 hr in fresh culture medium, and then plated for toxicity and mutagenicity assays. Mutation was determined by resistance to 20mug 8-azaguanine per ml. In this assay system, the S15 fraction and cofactors by themselves were not toxic to the cells; dose-related mutagenicity and cytotoxicity were induced by N-nitrosodimethylamine (DMN) only in the presence of the S15 fraction and cofactors. Pretreatment of rats with phenobarbitone led to an approximately 2-fold increase in the mutation rate over that with tissues from untreated rats with concentrations of DMN from 10 to 50 mM, while aminoacetonitrile pretreatment reduced the mutagenic effect. Methylcholanthrene pretreatment resulted in an increase in the mutation frequency with a higher concentration of DMN (50mM). Various other nitrosamines were also assayed in the presence or absence of the S15 fraction from phenobarbitone-pretreated rats and a reduced nicotinamide adenine dinucleotide phosphate-generating system. With the exception of N-nitrosomethylphenylamine, the carcinogenic nitrosamines (DMN, N-nitrosodiethylamine, N-nitrosodi-n-propylamine, N-nitrosodi-n-butylamine, N-nitrosodi-n-pentylamine, N-nitrosomethyl-n-propylamine, N-nitrosomorpholine, N-nitrosopyrrolidine, N-nitroso-N'-methylpiperazine, and N-nitrosomethylphenylamine) were mutagenic to the V79 Chinese hamster cells in the presence of the S15 fraction and cofactors. Neither N-nitrosodiphenylamine nor N-nitrosomethyl-tert-butylamine had a mutagenic effect. These findings show that chemical carcinogens can be tested for mutagenicity in cultured mammalian cells in the presence of a metabolic activation system. The results are discussed in relation to the carcinogenicity and mutagenicity of these compounds in other test systems.

Acetonitriles↗
PubMed1988

[N-nitrosamines in gastric juice of subjects from high incidence area of esophageal cancer].

A total of 353 samples of gastric juice was collected from Lin-xian subjects who were examined by endoscopy. NDMA, NDEA, NMBzA, Npyr, Npip, NSAR and other unknown compounds were detected in the fasting gastric juice. NMBzA, Npyr, Npip and NSAR can induce esophageal cancer in animals. Among the concentrations of N-Nitrosamines in gastric juice, the level of NDMA was the highest, its mean value 17.09 ppb; the level of NDEA stood next with a mean value of 6.95 ppb; the amounts of NMBzA, Npyr and Npip were 4.77, 2.45 and 1.30 ppb, respectively. A positive correlation was found between the amount of N-Nitrosamines in gastric juice and the various lesions in the esophageal epithelium of the subjects, the amount of N-Nitrosamines in gastric juice from subjects with normal esophageal epithelium was lower than that from subjects with marked dysplasia or carcinoma of esophagus. This finding lends further support to their possible involvement in esophageal cancer development.

Carcinogens↗
PubMed1988

[Effect of copper and zinc on the metabolism of N-nitrosamine and the activity of cytochrome P-450 in the liver of rats].

The effect of copper and zinc on the metabolism of N-nitrosamine and activity of cytochrome P-450 in the liver of rats was studied. Copper and zinc enhanced obviously the activity of cytochrome P-450 in the liver. The level of cytochrome P-450 in the liver of control rats was 0.64 nmol/mg protein but that in the liver of rats treated with copper or zinc was 1.31 and 1.17 nmol/mg protein. There was a significant difference between the two groups (P less than 0.01-0.001). The activity of demethylase reflected the metabolic level of N-nitrosamine. In the control group, metabolic level of N-dimethyl-nitrosamine, N-methyl-N-butylacetonylnitrosamine and nitrosopyrrolidine was markedly higher than the copper and zinc groups. It is indicated that copper and zinc inhibit obviously the activity of demethylase, resulting in reduction of the metabolic activation of N-dimethylnitrosamine, N-methyl-N-butylacetonylnitrosamine and nitrosopyrrolidine. The role of copper and zinc in the chemical carcinogenesis is discussed.

Animals↗
PubMedDate not supplied

Determination of volatile N-nitrosamines in frankfurters containing minced fish and surimi.

A method was developed to quantitatively measure volatile N-nitrosamines, particularly N-nitrosodimethylamine (NDMA), in cured minced fish or surimi-meat frankfurters. This method is free from artifact formation. First, 2 dry solid-phase extraction columns are prepared. Solvent is passed through the top column containing the fish-meat into a second column containing acid Celite. The eluate from the Celite column is then passed through a third column containing silica gel. Nitrosamines are eluted from the acid Celite column and then from the silica gel column into the same receiver. Recovery of the internal standard, N-nitrosoazetidine, added at the 10 ppb level, was 86.5%. In addition, a few samples of nitrite-treated salmon (lox) were also tested for N-nitrosamines. The results show that the method is applicable to samples containing nitrite-treated fish and fish-derived products.

Animals↗
PubMed1986

Malignant transformation of human fetal lung fibroblasts induced by nitrosamine compounds in vitro.

This report, for the first time, demonstrates that diethyl-nitrosamine (NDEA) and a new nitrosamine compound-N-1-methylacetonyl-N-3-methylbutyl-nitrosamine (MAMBNA), which are suspicious carcinogens of esophageal cancer (EC) in Linxian, Henan Province, are able to cause the malignant transformation (altered morphology, extended life span, anchorage independent growth, invasiveness, tumorigenicity, etc.) of normal diploid fibroblasts derived from human fetal lung. Besides, the preselection for clonogenic cells, which seem to be more readily to be transformed, in soft agar before carcinogen treatment, could be considered as one of the useful ways in establishment of a model system of malignant transformation of human fibroblasts in vitro.

Cell Transformation, Neoplastic↗
PubMedDate not supplied

Improved method for determination of volatile nitrosamines in baby bottle rubber nipples and pacifiers.

A method is described for determining volatile nitrosamines in baby bottle rubber nipples and pacifiers. The method consists of overnight soaking of the sample with dichloromethane in the presence of propyl gallate, an inhibitor for artifactual formation of nitrosamines; extraction with dichloromethane using an ambient temperature column procedure; distillation from aqueous alkali; extraction of the aqueous distillate with dichloromethane and concentration of the extract using a Kuderna-Danish concentrator; and final analysis by gas chromatography with detection by thermal energy analyzer. Major improvements over other published methods include a simpler extraction, a more efficient distillation and concentration to minimize losses, and incorporation of propyl gallate inhibitor as well as of a test to detect unsuitable dichloromethane solvent that otherwise might lead to artifactual formation. The method is highly accurate (approximately 90% recovery) and precise (av. CV = 4.7% at greater than 9 ppb levels) and is applicable to determination of nitrosamines in both rubber- and plastic-based products.

Chemical Phenomena↗
PubMed1987

Syncarcinogenesis at low exposure levels of three nitrosamines with a common target of carcinogenic action: preliminary results.

The carcinogenic activities of N-nitrosodiethylamine (NDEA), N-nitrosopyrrolidine (NPYR) and N-nitrosodiethanolamine (NDELA) and of the combination of the three nitrosamines was determined in Sprague-Dawley rats at three logarithmically spaced exposure levels. The highest doses of the individual nitrosamines and of their combination, chosen so as to induce low specific incidences of liver tumours following life-long administration, resulted in median survival times for all treated groups of more than 30 months. The macroscopically determined incidences of liver tumours were 1% in control rats, 45%, 4% and 4% following administration of NDEA, 14%, 3% and 1% following administration of NPYR, 6%, 5% and 1% following administration of NDELA and 12%, 4% and 3% following the combined administration of all three nitrosamines. These results indicate linear, additive carcinogenicity with respect to their common target organ in the dose range investigated.

Animals↗