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PubMed2005

Differences in susceptibility to N-butyl-N-(4-hydroxybutyl)nitrosamine-induced urinary bladder carcinogenesis between SD/gShi rats with spontaneous hypospermatogenesis and SD/cShi rats with spontaneous hydronephrosis.

Differences in susceptibility to N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN)-induced urinary bladder carcinogenesis between two substrains of male Sprague-Dawley rats were examined. One substrain was SD/gShi, which has spontaneous hypospermatogenesis, and the other was SD/cShi, which is a sister strain of SD/gShi, and has normal testis but spontaneous hydronephrosis. SD/gShi rats had a lower incidence of urinary bladder tumors and had lower 5-bromo-2'-deoxyuridine labeling indices in the urinary bladder epithelium than SD/cShi rats when BBN was given. SD/gShi rats had significantly lower urinary concentrations of N-butyl-N-(3-carboxypropyl)nitrosamine (BCPN), which is a metabolite and proximate carcinogen of BBN. In vitro analysis also showed significantly less BCPN formation, using an S9 mix derived from the liver and kidney, in SD/gShi rats than in SD/cShi rats. BCPN formation in vitro was markedly inhibited by non-selective cytochrome P450 (CYP) inhibitors, but not alcohol dehydrogenase inhibitor. However, analysis of CYP proteins including hepatic CYP1A1/2, 2B1/2, 2E1, and 3A2 and renal CYP2E1 and 3A2 revealed no significant variation in levels in either tissue in the groups. There were also no significant intergroup differences in the mutagenicity of carcinogens, including heterocyclic amines and N-nitrosamines, activated by CYP1A1/2 and CYP2E1 and/or CYP2B1/2, respectively. These results suggest that SD/gShi rats are less susceptible to BBN, possibly because less BCPN is produced by CYP isoforms other than those investigated. A contribution of CYP4B1 to the strain difference is also possible.

Animals↗
PubMed1991

[Studies of pickled vegetables and cause of esophageal cancer in Linxian. II. Determination of nitrosamines and their precursors].

Pickled vegetables are daily food consumed in the high-risk areas for esophageal cancer in China. We analyzed the nitrosamine content of Linxian pickles by GC/TEA and found that trace amounts of six nitrosamines (NDMA, NDEA, NMBA, NMAMBA, NDPA, NPYR) were present, with the highest concentrations being NDMA and NDEA (1.7 and 1.9 micrograms/kg wet weight respectively). The average level of nitrosamine precursors, such as nitrate (111.22 mg/L), nitrite (0.152 mg/L) and secondary amines (4.223 mg/L), in pickled vegetables were determined, and their pH values ranged from 3 to 5.

Diethylnitrosamine↗
PubMed1987

Cell cycle-dependent initiation of hepatocarcinogenesis in rats by methyl(acetoxymethyl)nitrosamine.

Hepatocyte sensitivity to initiation of carcinogenesis was studied as a function of the cell cycle phase in which damage was incurred. Hepatocytes were stimulated to proliferate by a two-thirds partial hepatic resection, and their proliferation was synchronized further by postsurgical treatment with hydrocortisone. Groups of male F344 rats were given a single administration of methyl(acetoxymethyl)nitrosamine, a highly reactive methylating agent, at various times after two-thirds partial hepatic resection when hepatocytes were in defined phases of the cell cycle. Beginning 3 wk after the treatment and for 37 wk thereafter, rats were fed a diet containing 0.05% phenobarbital to promote the expression of initiated hepatocytes. At 45 wk after treatment with carcinogen hepatocytic neoplasms were enumerated. The greatest yield of neoplasms (5.4 per liver) was observed in the group treated 16 h after two-thirds partial hepatic resection or at the time when proliferating hepatocytes began to enter the S phase of the cell cycle. The least yield of neoplasms (0.8 per liver) was identified in the group treated with methyl(acetoxymethyl)nitrosamine when hepatocytes were early in G1. In the proliferating hepatocytes sensitivity rose continuously during G1 to a peak at the G1-S border and then fell continuously as hepatocytes traversed S, G2, and M. This pattern of response could not be attributed to variation in hepatic esterase which activates methyl(acetoxymethyl)nitrosamine or to variation in methylation of DNA. The results support a model in which carcinogen-induced genetic alterations, occurring at the time of or soon after damaged cells enter the S phase, represent irreversible events that contribute to the initiation of carcinogenesis.

Animals↗
PubMed1985

Use of 3,4-dichlorobenzenethiol as a trapping agent for alkylating intermediates during in vitro metabolism of nitrosamines.

Our studies using 3,4-dichlorobenzenethiol as a probe for methylating agent production during exposure of N-nitrosodimethylamine to rat liver S-9 preparations produced results different from those of an investigation reported in the literature. Methyl-3,4-dichlorophenyl thioether was detected, but the quantities found were not significantly different from the background levels of methylation product detected in the absence of nitrosamine. Only about 10% of the thioether isolated after incubating N-nitrosodi[14C]methylamine as substrate was radioactive. The results indicate that the majority of the methyl groups transferred to the sulfur nucleophile in our experiments came from components of the incubation mixture other than the nitrosamine. Some artifactual methylation was also associated with the analytical procedure. We conclude that 3,4-dichlorobenzenethiol should be used with caution in studies of alkylation during the in vitro metabolism of carcinogenic nitrosamines.

Animals↗
PubMed1983

Mutagenicity of potassium alkanediazotates and their use as model compounds for activated nitrosamines.

The mutagenicity of a series of potassium alkanediazotates in the Ames assay was studied. These compounds were isolated as solids and are soluble in dimethyl sulfoxide. Upon addition to water, they form diazohydroxides (which are postulated intermediates in the decomposition of alpha-hydroxylated nitrosamines). The diazohydroxides decompose to electrophilic intermediates which may react with macromolecules or water. In the Ames assay, potassium diazotates produced his+ revertants in Salmonella typhimurium strains TA 100 and TA 1535 but not in strains TA 98, TA 1537, or TA 1538. Methane, methane-d3, ethane, propane, and phenylmethanediazotates were mutagenic in strain TA 100, and all diazotates with the exception of phenylmethanediazotate, produced revertants in TA 1535. The order of mutagenic potency of these compounds was: methane approximately equal to methane-d3 greater than ethane, greater than phenylmethane (TA 100) greater than propane greater than phenylmethane (TA 1535) = 0. All diazotates were direct-acting mutagens and produced revertants even when no liver 9000 X g supernatant (S9) fractions were present. S9 fractions inhibited the mutagenicity of potassium diazotates, and equivalent concentrations of S9 fractions (3 mg protein per plate) from either rat or hamster liver, whether induced or not, were equally effective. Bovine serum albumin was not as effective as S9 fractions in inhibiting diazotate mutagenesis, but heat-inactivated (70 degrees for 20 min) S9 fractions were as inhibitory of methanediazotate mutagenicity as native S9 fractions were at low protein concentrations. The half-lives of mutagenicity of methane- and ethanediazotates in aqueous solutions were identical (less than or equal to 15 sec); after less than 2 min in solution, these diazotates were rendered completely inactive. The implications of these studies for mechanisms of nitrosamine action and the use of potassium alkanediazotates as model compounds for activated nitrosamines are discussed.

Animals↗
PubMedDate not supplied

Supercritical fluid extraction of volatile N-nitrosamines in fried bacon and its drippings: method comparison.

N-Nitrosopyrrolidine (NPYR) and N-nitrosodimethylamine (NDMA), known animal carcinogens, are consistently formed in bacon during frying. As a result, commercial bacon has been subject to regulatory monitoring and compliance for the past 20 years to ensure that N-nitrosamines do not exceed the 10 ppb volatile level. Currently, time-consuming distillation-solvent extraction and solid-phase extraction (SPE) methods are used for this purpose. With an emphasis on reducing solvent use, we investigated supercritical fluid extraction (SFE) using supercritical carbon dioxide (SC-CO2) for isolation of volatile nitrosamines common to fried bacon. Eighteen fried bacon samples were analyzed for NPYR and NDMA by SFE, SPE, mineral oil distillation (MOD), and low-temperature vacuum distillation (LTVD) methods, using the same gas chromatographic-chemiluminescence detection (thermal energy analyzer) conditions. The range of values for SFE was 0.7 to 20.2 ppb for NPYR and none detected (ND) to 2.4 ppb for NDMA. Analysis of variance of the NPYR data showed a significant difference (p < 0.05) between SFE and SPE results and significant differences between these and those obtained by MOD and LTVD. Overall, SFE was superior to the other methods with the highest recoveries, best repeatability, rapidity of analysis, and solvent-sparing characteristics. Similar results were obtained for SFE after comparison with distillation and SPE methods for determining the same nitrosamines in fried bacon drippings.

Analysis of Variance↗
PubMed1998

High susceptibility of p53(+/-) knockout mice in N-butyl-N-(4-hydroxybutyl)nitrosamine urinary bladder carcinogenesis and lack of frequent mutation in residual allele.

The loss of p53 functions is considered to compromise the growth-suppression machinery of the cell and facilitate neoplastic change. In humans, genetic alteration in the p53 gene is one of the most frequently observed molecular changes in tumors, including urinary bladder carcinomas. We have investigated the susceptibility of heterozygote p53 knockout mice to N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in terms of urinary bladder tumor induction. Both p53(+/-) knockout mice and C57BL/6 original parent strain were administered 0, 0.002, 0.004, 0.0075 and 0.025% BBN in the drinking water for 20 weeks. As compared with the C57BL/6 strain, greater lesion yields were observed in knockout mice after 20 weeks of treatment. Transitional cell carcinomas were found in 9 (75%) and 12 (100%) of each 12 mice of the 0.0075 and 0.025% BBN treatment groups, respectively, whereas only 1 (11%) and 6 (67%) of each 9 of the C57BL/6 mice demonstrated tumors. Preneoplastic lesions (dysplasia) were also observed more frequently in the lower dose groups in the knockout mice than C57BL/6 mice. PCR single-strand conformation polymorphism analysis followed by DNA direct sequencing of the p53 gene (exons 5-8) extracted from bladder tumors demonstrated mutations in 3 of 11 (27.3%; exon 7) and 8 of 29 (27.6%; exons 5-8) tumors in C57BL/6 and knockout mice, respectively. There was no significant difference in the mutation rates at the residual p53 gene between the two cases. All mutations observed in knockout mice were restricted to the normal allele, and none were present in the gene-targeted null allele. In a separate experiment, 5-bromo-2'-deoxyuridine labeling indices after treatment with BBN for 2 or 4 weeks were significantly higher in knockout mice than wild-type mice. Measurement of the urinary concentration of N-butyl-N-(3-carboxypropyl)nitrosamine, a proximate carcinogenic metabolite, revealed no significant differences between knockout and original parent strain after administration of 0.0075% BBN in the drinking water for 4 weeks. In conclusion, knockout mice are distinctly more sensitive to urinary bladder carcinogenesis induced by BBN than their original parent strain, as evidenced by elevated DNA synthesis during carcinogen administration and an increased tumor yield. The high susceptibility of p53 knockout mice appeared to be related to the high level of cell proliferation rather than that of N-butyl-N-(3-carboxypropyl)nitrosamine in the urine or that of mutations at the p53 gene.

Alleles↗
PubMed1999

Elevated mortality from nonalcohol-related chronic liver disease among female rubber workers: is it associated with exposure to nitrosamines?

BACKGROUND: Despite several case reports describing liver toxicity of nitrosamines and the fact that some N-nitroso compounds are used to induce cirrhosis of the liver in animal models, this association has not been investigated in epidemiological studies. METHODS: A cohort of 2,875 female rubber workers who were active on January 1, 1976, or hired thereafter, and who had been employed for at least 1 year in one of five plants producing tires or technical rubber goods was followed for mortality from January, 1976, through December, 1991. Work histories were reconstructed using routinely documented "cost center codes" and classified into six work areas. Age and calendar year standardized mortality ratios (SMR) and 95% confidence intervals (95% CI) were calculated and stratified by plant, work area, year of hire, and years of employment in the respective work area. RESULTS: The excess mortality from cirrhosis of the liver was most pronounced for nonalcohol-related cirrhosis of the liver (ICD-9 571.4-571.9: 10 deaths, SMR 202; 95% CI 97-372). Mortality from alcohol-related cirrhosis of the liver (ICD-9 571.0-571.3: 3 deaths, SMR 153; 95% CI 31-446) and from other alcohol-related diseases (organic psychoses, injury, and poisoning) was not statistically significantly elevated. All 10 cases of nonalcohol-related cirrhosis had worked in production of technical rubber goods (SMR 279; 95% CI 134-514) and risks increased with earlier years of hire and with longer duration of employment in this work area. DISCUSSION: Although our results must be interpreted with caution, they suggest that the observed excess deaths from cirrhosis of the liver are associated with occupational risk factors. In light of additional evidence from case reports and animal data, exposure to nitrosamines may be a plausible risk factor for the observed excess mortality.

Adult↗
PubMed1991

Aerial oxidation of hydrazines to nitrosamines.

When 1,1-dimethylhydrazine and N-aminopiperidine were deliberately exposed to air substantial amounts of the corresponding carcinogenic nitrosamines were formed. Unoxidized samples of 1,1-dimethylhydrazine were not mutagenic while oxidized samples (which contained much higher levels of nitrosamines) were mutagenic. Both unoxidized and oxidized samples of N-aminopiperidine were mutagenic.

1,2-Dimethylhydrazine↗
PubMed2003

Malignant transformation of human bronchial epithelial cells with the tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone.

Sufficient evidence has demonstrated that cigarette smoking is causally associated with various types of human cancers. In the United States, about 90% of deaths from lung cancer among men and 79% of those among women are associated with smoking. Tobacco-specific nitrosamines are formed from nicotine and related tobacco alkaloids and are the most carcinogenic compounds of tobacco smoke. The most potent N-nitrosamine contained in tobacco smoke is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, NNK. In the our study, the oncogenic transforming effects of graded doses of NNK were examined using papillomavirus-immortalized human bronchial epithelial cells. Growth kinetics, saturation density, resistance to serum-induced terminal differentiation, anchorage independent growth and tumorigenicity in nude mice were used to investigate the various stages of transformation in bronchial epithelial cells. We show here that immortalized human bronchial epithelial cells in culture can be malignantly transformed by treatment with NNK (100 microg/ml or 400 microg/ml) for 7 days. Transformed cells produced progressively growing subcutaneous tumors upon inoculation into nude mice. Immunofluorescence staining for keratin expression confirmed the epithelial nature of the tumor cells. Increased expression of p16, beta-catenin and PCNA in the established cell lines were detected by immunofluorescence staining and quantified by confocal microscopy. These data suggested that NNK can induce malignant transformation of human bronchial epithelial cells, and the tumor cell lines established are useful models in investigating the carcinogenic mechanism(s) of NNK.

Animals↗
PubMed1987

Volatile nitrosamine levels in common foods from Tunisia, south China and Greenland, high-risk areas for nasopharyngeal carcinoma (NPC).

On the basis of anthropological pilot studies on diet in Tunisia, south China and Greenland, food items consumed frequently by these populations at high risk for NPC were analysed for volatile nitrosamines using gas chromatography combined with a thermal energy analyzer. Relatively high levels of N-nitrosodimethylamine (NDMA), N-nitrosopyrrolidine (NPYR) and N-nitrosopiperidine (NPIP) were detected in Tunisian stewing base ("Touklia") and dried mutton preserved in olive oil ("Qaddid"). NDMA was also detected at levels ranging from trace amounts to 133 micrograms/kg in several Chinese salted and dried marine fish and in Greenland dried, unsalted fish preparations. NPYR and NPIP were also occasionally detected in several vegetables fermented in brine collected in Tunisia and China. The possible role of nitrosamines in the etiology of NPC is discussed.

China↗
PubMed1991

Opisthorchis viverrini infestation and endogenous nitrosamines as risk factors for cholangiocarcinoma in Thailand.

Cholangiocarcinoma (CCA) is one of the most common cancers in north-east Thailand and has been associated with infestation by the liver fluke Opisthorchis viverrini (OV). Two samples of 12-hr overnight urine (after dosing with proline and ascorbic acid or proline alone) were collected from 20 inhabitants from each of 5 contrasting incidence areas for CCA. The incidence of CCA was not correlated with either the amount of NPRO or other nitrosamino acids, endogenous nitrosation potential (difference in NPRO levels between proline dose and proline and ascorbic dose), or nitrate level. However, when urinary levels of nitrosamino acids were compared in subjects living in high-risk areas, subjects who were positive for OV antibody excreted significantly more (p less than 0.01) NPRO (12.3 +/- 18.7 micrograms/12 hr) after proline ingestion than those who were negative (3.5 +/- 3.2 micrograms/12 hr). After ingestion of ascorbic acid, the NPRO levels in the positive subjects were significantly reduced (p less than 0.01) to 2.4 +/- 2.0 micrograms/12 hr, suggesting that endogenous nitrosation of proline was inhibited. Thus, endogenous nitrosation potential estimated from the difference between NPRO and the sum of nitrosamino acids excreted in the 2 urine samples was significantly higher in subjects positive for the OV antibody. Small amounts of pre-formed nitrosamines were found in fermented fish and pork food items, which are consumed frequently in the high-risk area for CCA. These results suggest that the interaction between chemical carcinogens, especially nitrosamines, and OV infestation may play a role in the development of cholangiocarcinoma in Thailand.

Adenoma, Bile Duct↗
PubMedDate not supplied

Protective effects of isothiocyanates towards N-nitrosamine-induced DNA damage in the single-cell gel electrophoresis (SCGE)/HepG2 assay.

The aim of this study was to investigate the protective effect of isothiocyanates towards N-nitrosamine-induced DNA damage in the single-cell gel electrophoresis (SCGE)/HepG2 assay. None of the isothiocyanates (ITCs) concentrations tested in the presence or absence of formamidopyrimidine-DNA glycosylase (Fpg) caused DNA damage per se. Combined treatments of HepG2 cells with phenethyl isothiocyanate (PEITC), allyl isothiocyanate (AITC) or indol-3-carbinol (I3C) and N-nitrosopyrrolidine (NPYR) or N-nitrosodimethylamine (NDMA) reduced the genotoxic effects of the N-nitrosamines in a dose-dependent manner. The protective effect of the three ITCs tested was higher towards NPYR-induced oxidative DNA damage than against NDMA. The greatest protective effect towards NPYR-induced oxidative DNA damage was shown by I3C (1 microM, 79%) and by PEITC (1 microM, 67%) and I3C (1 microM, 61%) towards NDMA (in presence of Fpg enzyme). However, in absence of Fpg enzyme, AITC (1 microM, 72%) exerted the most drastic reduction towards NPYR-induced oxidative DNA damage, and PEITC (1 microM, 55%) towards NDMA. Our results indicate that ITCs protect human-derived cells against the DNA damaging effect of NPYR and NDMA, two carcinogenic compounds that occur in the environment.

Anticarcinogenic Agents↗
PubMedDate not supplied

Protective effects of isothiocyanates towards N-nitrosamine-induced DNA damage in the single-cell gel electrophoresis (SCGE)/HepG2 assay.

The aim of this study was to investigate the protective effect of isothiocyanates towards N-nitrosamine-induced DNA damage in the single-cell gel electrophoresis (SCGE)/HepG2 assay. None of the isothiocyanates (ITCs) concentrations tested in the presence or absence of formamidopyrimidine-DNA glycosylase (Fpg), caused DNA damage per se. Combined treatments of HepG2 cells with phenethyl isothiocyanate (PEITC), allyl isothiocyanate (AITC) or indol-3-carbinol (I3C) and N-nitrosopyrrolidine (NPYR) or N-nitrosodimethylamine (NDMA) reduced the genotoxic effects of the N-nitrosamines in a dose-dependent manner. The protective effect of the three ITCs tested was higher towards NPYR-induced oxidative DNA damage than against NDMA. The greatest protective effect towards NPYR-induced oxidative DNA damage was shown by I3C (1 microm, 79%) and by PEITC (1 microm, 67%) and I3C (1 microm, 61%) towards NDMA (in the presence of Fpg enzyme). However, in the absence of Fpg enzyme, AITC (1 microm, 72%) exerted the most drastic reduction towards NPYR-induced oxidative DNA damage, and PEITC (1 microm, 55%) towards NDMA. The results indicate that ITCs protect human-derived cells against the DNA damaging effect of NPYR and NDMA, two carcinogenic compounds which occur in the environment.

Antimutagenic Agents↗
PubMed1990

Mutational specificities of environmental carcinogens in the lacl gene of Escherichia coli. III: The cyclic nitrosamine N-nitrosopyrrolidine is a complex mutagen.

The mutational specificity of the cyclic nitrosamine N-nitrosopyrrolidine (NPYR) was determined through the DNA sequence characterization of 33 lacl-d mutations of Escherichia coli. Base substitution was the predominant class of mutation induced (91%). The majority of these (64%) occurred at GC base pairs, in accordance with the predicted significance of NPYR-derived guanine adducts. In addition, this nitrosamine efficiently produced other kinds of base substitution events as 11 of the 33 mutations occurred at AT base pairs. Deletion, frameshift, and duplication events were also recovered. The complexity of the NPYR mutational spectrum appears to be consistent with the suggestion that this compound acts through both direct and indirect mutational pathways.

Carcinogens, Environmental↗
PubMed1992

Mutational specificities of N-nitrosamines in a host-mediated assay: comparison with direct-acting N-nitroso compounds in vitro and an approach to deducing the nature of ultimate mutagens in vivo.

The mutational activities and specificities of several N-nitrosamines in Salmonella recovered from mouse liver in the host-mediated assay (HMA) were compared with the specificities of related direct-acting N-nitroso compounds in vitro. The specificities of the direct-acting methyl, ethyl, propyl, and 2-hydroxypropyl compounds were all different and presumably are attributable to the DNA adducts resulting from the corresponding alkyldiazonium or carbonium ions. Introduction of a 2-hydroxyl group greatly influenced the mutational specificity. The 2-oxopropyl compound showed the same specificity as the methyl compound. This result is consistent with one of the known breakdown pathways of the oxopropyl diazonium ion (or related reactive species), which leads to a methyl diazonium ion. The N-nitrosodialkylnitrosamines N-nitrosodimethylamine (NDMA), N-nitrosodiethylamine (NDEA), and N-nitrosodipropylamine (NDPA), which all require metabolic activation, showed specificities in the HMA similar to those of their direct-acting counterparts. The cyclic nitrosamine N-nitrosopyrrolidine was weakly active in the HMA, although its direct-acting derivative was a potent mutagen in vitro. The results for NDMA and NDEA were consistent with most previous studies of the metabolism of these compounds in vivo. However, NDPA can yield methylating, and probably hydroxypropylating, species in addition to propyldiazonium ion. As the specificity of NDPA was similar to that of a propylating agent, NDPA appears to lead to genotoxic products in the mouse liver mainly by direct alpha-hydroxylation. The initial results described here indicate that mutational specificity in the HMA can be used to deduce metabolic pathways leading to genotoxic products when the appropriate proximate mutagens are available as standards. Furthermore, we observed a reasonable correlation between potency in the HMA and hepatocarcinogenesis.

Animals↗
PubMedDate not supplied

Systemic genotoxic effects of tobacco-related nitrosamines following oral and inhalational administration to Sprague-Dawley rats.

An ex vivo model to detect nonspecific DNA damage in different rat tissues has been developed and employed to study systemic properties of tobacco-specific N-nitrosamines. One hour after treatment of rats with the carcinogens, primary, intact cells were isolated from various organs. Viability of the cells was monitored by trypan blue exclusion. Genotoxicity was determined by alkaline elution, in situ nick translation or microgel electrophoresis. We found that oral application of 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces genotoxic effects in the liver (3.125-50 mg/kg), whereas N-nitrosonornicotine (NNN) is only moderately active (50-100 mg/kg). Furthermore, oral administration of NNK, NNN, and of N-nitrosodimethylamine (NDMA), induces DNA damage in the nasal cavity. In peripheral blood lymphocytes genotoxicity of NDMA (less than 2 mg/kg), but not of NNK (50 mg/kg), was observed. NDMA and NNK are just as genotoxic in the liver when administered by inhalation as orally (effective doses: 0.1-1 and 50 mg/kg, respectively). For human cancer, these results indicate that in addition to the susceptibilities in local organs (oral cavity after snuff dipping and lung after tobacco smoke inhalation), these nitrosamines also pose a risk systemically for more remote organs.

Administration, Inhalation↗
PubMed1977

Occurrence of volatile N-nitrosamines in animal diets.

46 samples of commercially available diets for experimental animals have been analysed for their content of volatile N-nitrosamines by use of a nitrosamine-specific detection method (TEA-detector). 80% of all analysed samples were positive for N-nitrosodimethylamine with a maximum content of 79 ppb (microgram/kg) found in one sample. 59% of the samples were positive for N-nitrosopyrrolidine with 26 ppb as highest content. In 3 samples trace quantities (less than 1 ppb) of N-nitrosodiethylamine were found, one sample contained N-nitrosopiperidine (4 ppb).

Animal Feed↗