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PubMed1978

The intake of nitrate, nitrite and volatile N-nitrosamines and the occurrence of volatile N-nitrosamines in human urine and veal calves.

A hundred samples of total diets, 19 samples of cheese (mainly Dutch), a total of 30 samples of muscle, fat liver, kidney, blood and fried meat from experimental veal calves (fed daily with 0.6 or 300 mg of potassium nitrate per kg b.w.) and 14 samples of urine of patients medicated with massive amounts of ammonium nitrate (up to an equivalent of 180 mg potassium nitrate per kg b.w.) have been analysed with GC-TEA for their content of the following N-nitrosamines: NDMA, NDEA, NDPA, NDBA, NPIP, NPYR and NMOR. NDMA was frequently found, but always in the sub micrograms per kg range, except for two diets (1.2 and 1.7 microgram/kg). Other N-nitrosamines were sporadically found in the same concentration range, except for one diet (NPYR, 1.9 microgram/kg). No correlation was found between NDMA content and the composition of diets or the nitrate load of patients or veal calves. Mean daily intake of NDMA, potassium nitrate and sodium nitrite from total diets was calculated to be 0.5 microgram, 215 mg and 7.7 mg respectively. N-nitrosamine recoveries from the various samples were determined mostly at the 1 microgram/kg level. Contents of potassium nitrate and sodium nitrite are reported for 124 samples of various vegetables, 94 samples of canned baby food and 48 samples of human saliva, collected at various times after the intake of meals. Some kinds of vegetables showed high to very high nitrate contents, for example, purslane, red beets, spinach and lettuce. Only traces of nitrite were found in the vegetables. Salivary nitrite content was shown to be highly dependent on the dietary intake of nitrate and increased up to 60 times its initial value after the consumption of vegetable-rich meals.

Adult↗
PubMed1982

O-alkylation of N-nitrosamines. Transalkylation of N-nitrosamines and formation of electrophilic intermediates.

Ring closure of appropriately beta-substituted nitrosamines leads to the formation of dihydrooxadiazolium ions. These relatively stable, crystalline compounds react with nucleophiles, either at the position of the beta-substituent or by displacement of an alkyl group bound to the nitrogen. These compounds are intramolecular varients of alkoxydiazenium ions, which are formed by the O-alkylation of nitrosamines with a variety of agents, including alkyl-fluorosulfonates. The alkoxydiazenium ions are also stable, crystalline solids. They react with nucleophiles usually by displacement at the O-alkyl group. One exception to this, however, is the reaction of 3,4-dichlorothiopheno in organic solvents to form thioethers by O-dealkylation and N-dealkylation. The by-products of the dealkylations are the corresponding nitrosamines. The aqueous reactions of 3,4-dichlorothiophenol are slower and pH-dependent. In acidic media, 3,4-dichlorothiophenol reacts only at the O-alkyl groups, whereas in weakly alkaline media, a little O- and N-dealkylation is observed, together with considerable base-catalysed decomposition of the alkoxydiazenium ions.

Alkylation↗
PubMed1987

International Commission for Protection against Environmental Mutagens and Carcinogens. ICPEMC Working Paper No. 15/6. Effect of ethanol on nitrosamine metabolism and distribution. Implications for the role of nitrosamines in human cancer and for the influence of alcohol consumption on cancer incidence.

Alcohol consumption is associated with an increase in the incidence of cancers of several sites, including oesophagus, larynx and mouth. The mechanism of the induction of cancer by alcohol is not clear. Humans are exposed to a variety of carcinogenic N-nitroso compounds. Ethanol changes the pharmacokinetics of nitrosamines in rats particularly by decreasing the ability of the liver to metabolize them. A hypothesis is put forward that the influence of alcohol on human cancer is mediated by its effect on the metabolism and distribution of nitrosamines from the diet, from tobacco smoke and from endogenous synthesis.

Alcohol Drinking↗
PubMed1981

Nitrosamine-induced mutagenesis in Escherichia coli K12 (343/113). 1. Mutagenic properties of certain aliphatic nitrosamines.

The Escherichia coli K12 (343/113) test system developed by G. Mohn was used to detect the mutagenic activity induced by a group of aliphatic nitrosamines. Metabolic activation was incorporated into the assay by the addition of liver homogenates induced in either Sprague-Dawley rats or C3H mice with the addition of 0.1% phenobarbital to the drinking water. Nitrosodiethylamine (NDEA) was mutagenic upon metabolic activation and exhibited a preference to revert the missense mutation at the arginine locus. NDEA was also capable of inducing the forward mutation, selected as an ability to utilize galactose. NDEA was converted effectively into a mutagen in a time period of 30 min to 2 h. Metabolic activation with the mouse and rat liver preparations did not result in quantitative differences. Aliphatic nitrosamines that gave unexpected results with the Salmonella assay [4-10] were examined in the E. coli system. Nitrosodipropylamine (NDPA) and nitrosodiallylamine (NDAA) were mutagenic in both E. coli and Salmonella. Nitrosomethylethylamine (NMEA) was not mutagenic in Salmonella but was mutagenic in E. coli, and a strong carcinogen, nitrosomethylneopentylamine (NMNA), was not mutagenic in either assay. These results indicate the use of multiple genetic assays for the detection of genotoxic chemicals in our environment.

Escherichia coli↗
PubMed1988

Combined effects of L-ascorbic acid, citric acid or their sodium salts on tumor induction by N-butyl-N-(4-hydroxybutyl)nitrosamine or N-ethyl-N-(4-hydroxybutyl)nitrosamine in the rat urinary bladder.

L-Ascorbic acid, citric acid or their sodium salts (at levels equivalent to 5% sodium L-ascorbate) were fed in the diet simultaneously with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) or N-ethyl-N-(4-hydroxybutyl)nitrosamine (EHBN) (0.025% BBN or 0.021% EHBN) in the drinking water to male F344 rats for 20 weeks to determine whether urinary pH changes affect the carcinogenicity of BBN or EHBN. In the urine, pH was decreased in rats fed the acidic chemicals and increased in rats fed their corresponding sodium salts. Histopathologically, the incidences and numbers of preneoplastic and neoplastic lesions in groups treated with each test chemical were not different from those in control groups except for sodium citrate-treated groups in which induction of carcinomas was higher, resulting from increased intake of either carcinogen and also from increased urinary excretion of main carcinogenic metabolites. These results show that the test chemicals do not affect the carcinogenicity of BBN or EHBN on the rat urinary bladder when simultaneously administered despite significant differences in urinary pH.

Animals↗
PubMed1981

A correlation between mutagenic and carcinogenic potencies in a diverse group of N-nitrosamines: determination of mutagenic activities of weakly mutagenic N-nitrosamines.

The mutagenic activities of a diverse group of N-nitrosamines were measured in Salmonella typhimurium TA 100 under conditions designed to maximize metabolism of N-nitrosamines and enhance their mutagenic effects. These conditions were also chosen since some of the carcinogens were previously reported to be non-mutagenic or of questionable mutagenic activity and some only became mutagenic after the bacteria were exposed to a "threshold does" of metabolites. The mutagenic potencies spanned a range of 10(5)-fold and correlated well with semiquantitative carcinogenic potencies taken from the literature. This correlation appears to be the strongest yet reported for any particular class of compounds. In addition, the mutagenic activities of a number of carcinogens, previously reported to be non-mutagenic, were determined. Among the structural features necessary for high mutagenic activity in this group of compounds was a potential, unsubstituted methylating or ethylating group. Substitution of alkyl, hydroxyl, methoxyl, and cyano moieties at the alpha or beta carbon of these groups reduced mutagenic activity.

Carcinogens↗
PubMed1978

Focal suppression and induction of hyperplasia by the bladder carcinogens butyl(4-hydroxybutyl)nitrosamine and buty(3-carboxypropyl)nitrosamine in organ-cultured rat bladder epithelium.

The effects of the bladder carcinogens butyl(4-hydroxybutyl)nitrosamine (BBN) and butyl(3-carboxypropyl)-nitrosamine (BCPN) on proliferating transitional rat epithelium in organ culture were studied. At low to intermediate concentration ranges (0.5--2.9 mM), both compounds appeared to stimulate hyperplasia in some regions of epithelia. The major effect of both carcinogens, however, was to suppress hyperplasia in other regions of epithelia and, at higher concentrations (5--6 mM), to cause necrosis. For comparable concentrations, BBN was more effective in suppressing proliferation and causing necrosis than was BCPN.

Animals↗
PubMed1983

Relationship of urinary N-butyl-N-(3-carboxypropyl)nitrosamine to susceptibility of animals to bladder carcinogenesis by N-butyl-N-(4-hydroxybutyl)nitrosamine.

A simple and sensitive procedure is described for the quantitative determination of N-butyl-N-(3-carboxypropyl)nitrosamine (BCPN), the principal metabolite of the bladder carcinogen N-butyl-N-(4-hydroxybutyl)nitrosamine (BHBN-4), in urine. BCPN was analyzed by gas-liquid chromatography as its methyl ester after extraction with ethyl acetate from urine followed by esterification with diazomethane. Species and strain variations in susceptibility to bladder carcinogenesis induced by BHBN-4 are discussed in relation to the urinary excretions of BCPN, determined by the new procedure, after oral administration of the compound to rats (4 strains), mice, hamsters, and guinea pigs at a dose approximately equal to the daily dose used in chronic carcinogenicity assay.

Animals↗
PubMed1981

Bladder carcinogenesis in mice induced by N-butyl-N-(4-hydroxybutyl) nitrosamine and N-ethyl-N-(4-hydroxybutyl)-nitrosamine with reference to the effect of cyclophosphamide.

The carcinogenicities of N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) and N-ethyl-N-(4-hydroxybutyl) nitrosamine (EHBN) on the urinary bladder were compared in male BALB/c mice. The effect of cyclophosphamide (CPA) on the carcinogenicities was also investigated. The carcinogenic activity on the bladder mucosa of EHBN was similar to that of BBN, and there was no difference in the growth patterns, histological types or invasive characters of carcinomas induced by BBN and EHBN. Benign or malignant tumors of vascular origin developed in the urinary bladders of 15 mice treated with these carcinogens. The incidence of vascular tumors induced by EHBN was significantly higher than that of tumors induced by BBN. Intraperitoneal injections of CPA seemed to have no effect in the incidence of bladder carcinomas induced by these carcinogens, or on the development of vascular tumors in the bladder wall induced by EHBN.

Animals↗
PubMed1978

[On the carcinogenetic action of N-nitroso compounds. 7th communication: methyl-, trideuteromethyl-, ethyl-, n-propyl-, n-butyl-, acetoxymethyl-nitrosamine, and methyl-butyroxymethyl-nitrosamine (author's transl)].

The homologons alkyl-acetoxymethyl-nitrosamines were tested for carcinogenicity in SD rats. All compounds were found to be carcinogenic and induced within the same time carcinomas of the forestomach. The total doses necessary for induction of tumors are related to the length of the alkyl chain and hence to the watersolubility. These results are discussed.

Alkylation↗
PubMed2006

Occurrence and fate of nitrosamines and nitrosamine precursors in wastewater-impacted surface waters using boron as a conservative tracer.

Using boron as a conservative tracer of municipal wastewater effluents, a mass balance was developed to determine river flowrates that requires only wastewater discharge flowrates and boron concentrations in wastewater effluents and in the river upstream and downstream of these discharges. Furthermore, this method permits calculation of the percentage of the river deriving from wastewater. This method could be useful within river sections featuring no independent data regarding river discharge. We assessed the decay of nitrate and N-nitrosodimethylamine (NDMA) precursors within an engineered treatment wetland and, using our boron analysis technique to account for dilution, within the Quinnipiac River (CT). Although both decayed with several day half-lives, their slow decay indicates they can persist to impact downstream drinking water supplies. Concentrations of NDMA and N-nitrosomorpholine (NMOR) were measurable within the river, but concentrations of four other nitrosamines, their precursors, and NMOR precursors were not detectable.

Boron↗
PubMed1993

Hypothesis on the relationship between gastric cancer and intragastric nitrosation: N-nitrosamines in gastric juice of subjects from a high-risk area for gastric cancer and the inhibition of N-nitrosamine formation by fruit juices.

The concentration of N-nitrosamines (NNA) in gastric juice was determined as an indicator of intragastric N-nitrosation in 85 subjects from a high-risk area for gastric cancer (GC) to examine the relationship between N-nitroso compounds (NOC), pH and intragastric lesions under strictly controlled conditions. Mean gastric pH in subjects with GC or dysplasia (Group GD, 5.0 +/- 2.7) was higher than that from subjects with intestinal metaplasia (Group IM, 3.8 +/- 2.1, p = 0.068) and significantly higher than in those with normal mucosa or superficial gastritis (Group NS, 2.6 +/- 1.9, p < 0.001). No significant difference (p > 0.1) was found in total NNA concentrations between the three groups (GD 1.81 +/- 1.05 micrograms/l, IM 1.46 +/- 0.79 micrograms/l, NS 1.56 +/- 1.38 micrograms/l). However, two obvious peaks of nitrosation were observed at pH ranges of < 2.0 and 5.5-7.5. These observations were confirmed by using the N-nitrosoproline test in the same subjects under the same conditions (r = 0.772, p < 0.05). These results indicate that intragastric nitrosation can occur in both acidic and nearly neutral conditions. The first peak is related to acid-catalysed nitrosation (ACN) and the second is related to biologically catalysed nitrosation (BCN). According to these and other published results the hypothesis that there are two basic mechanisms, ACN and BCN, for intragastric N-nitrosation in humans is explored. Gastric carcinogenesis in high-risk areas is more likely to be related to intragastric NOC formed by ACN, compared to low-risk areas where it is more likely to be related to intragastric NOC formed by BCN. Fruit juices and orange peel significantly inhibited intragastric nitrosation by both ACN and BCN.

Adult↗
PubMedDate not supplied

International N-nitrosamine check sample programme: report on the performance in the 1st study dedicated to determination of N-nitrosamines in beer and malt.

Two samples, one beer and one malt, have been distributed to 55 laboratories in 15 countries, to be analysed for N-nitrosodimethylamine (NDMA) N-nitrosopyrollidine (NPYR) and N-nitrosoproline (NPRO) by the method of their choice. Results received from 35 laboratories demonstrated that at the low levels of contamination which may be encountered at present for NDMA in beer and malt, generally reliable data can be obtained in malt, but in beer, 20% of the results were discarded as outliers by the statistical test results. More variability was encountered for the analysis of NPYR. Only a limited number of results were provided for NPRO, which also showed greater variability.

Alcoholic Beverages↗
PubMed1993

Effect of streptozotocin diabetes on development of nitrosamine-induced pancreatic carcinoma when diabetes induction occurs after nitrosamine exposure.

Diabetes mellitus has been suggested as a possible risk factor for the development of pancreatic cancer in humans. Previous studies in our laboratory have shown, however, that streptozotocin (STZ) diabetes inhibits the development of cancer of the exocrine pancreas in hamsters when STZ is administered prior to treatment with the pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine (BOP). It has been reported by others that the concurrent administration of BOP and STZ enhances pancreatic carcinogenesis in hamsters. The purpose of the present study was to determine the effect of STZ diabetes on the development of BOP-induced pancreatic carcinoma when STZ is given following exposure to BOP. Groups of Syrian golden hamsters were treated with either BOP only (single s.c. injection, 40 mg/kg body wt at week 0), BOP (single s.c. injection, 40 mg/kg body wt at week 0) plus STZ (50 mg/kg body wt x3 daily i.p. doses at weeks 10, 20 or 30), STZ only (50 mg/kg body wt x3 daily i.p. doses at weeks 10, 20 or 30), or neither BOP nor STZ. The experiment was terminated at 40 weeks after BOP treatment. No significant difference was seen in the incidence of pancreatic cancer between those animals receiving BOP only at week 0 and those receiving BOP at week 0 plus STZ at weeks 10, 20 or 30 of the study. The results would appear to indicate that STZ diabetes, established after BOP tumor initiation, plays no apparent role in the modulation of pancreatic carcinogenesis.

Animals↗
PubMed1991

Chronic nitrosamine ingestion in 1040 rodents: the effect of the choice of nitrosamine, the species studied, and the age of starting exposure.

In parallel with a larger experiment on 4080 rats fed 16 different concentrations of N-nitrosodiethylamine (NDEA) or N-nitrosodimethylamine (NDMA) from 6 weeks of age, a variety of smaller experiments on a total of 1040 rodents were undertaken and are the subject of the present report. Three separate subjects were addressed. Studies of 16 different concentrations of N-nitrosopyrrolidine and N-nitrosopiperidine given from age 6 weeks onwards to small groups of rats yielded dose-response relationships for the effects of N-nitrosopyrrolidine on liver tumors and for those of N-nitrosopiperidine on tumors of the liver and upper gastrointestinal tract that resembled those seen for NDMA and NDEA, respectively, except that N-nitrosopyrrolidine and N-nitrosopiperidine were less potent [the respective dose rates needed to halve the proportion of tumorless survivors after 2 years of treatment being approximately 0.4 (males) and 0.6 (females) mg/kg adult body weight/day for each agent]. Alternatively, it was estimated that the risks to rats from lifelong exposure to 1 microgram/kg adult body weight/day of each agent might be about 0.1%, and that the risks to rats from lower doses would be proportionately less. Studies of 16 different concentrations of NDEA on small groups of female mice and female hamsters yielded the types of dose response that would be expected for upper gastrointestinal tumors, liver cell tumors, and Kupffer cell tumors in mice (no other types of liver tumor being produced, in contrast with previous reports) and for tracheal and liver cell tumors in hamsters (no clear effect on upper gastrointestinal tumors being apparent in hamsters). The dose rates needed to halve the proportion of tumorless survivors after 2 years of treatment were approximately 0.3 mg/kg adult body weight/day, i.e., 5 times that for the same agent in rats. In part, however, this may be because treatment started at an older age in these species. Studies were undertaken of the effects on esophageal and liver tumorigenesis of starting the treatment of rats with NDEA at 3 or at 20 weeks of age instead of at 6 weeks of age (as in the main experiment). Earlier treatment resulted in slightly greater dosage rates, if dosage was measured in mg/kg/day, and hence in a correspondingly more rapid yield of esophageal tumors, but the effect was not large. By contrast, an earlier start to treatment resulted, after a fixed duration of treatment, in animals having a 3-fold higher incidence rate of liver tumors, while a later start resulted in a 2-fold decrease.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗