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PubMed1987

Escherichia coli infection of the urinary bladder: induction of tumours in rats receiving nitrosamine precursors and augmentation of bladder carcinogenesis by N-nitrosobutyl (4-hydroxybutyl)amine.

Experimental introduction of Escherichia coli type 04 into the subserosa of the urinary bladder of female Fischer 344 rats produced chronic bacterial infection in more than 90% of animals. Groups of rats with bacterial infection were given sodium nitrate and either piperazine (Group 1) or dibutylamine (Group 2) in the drinking-water. Control, noninfected animals received nitrate and either piperazine (Group 3) or dibutylamine (Group 4). At 40 weeks, transitional-cell carcinomas of the bladder were detected in 9/30 rats in Group 1 compared to 0/34 in Group 3 (p less than 0.0005), and in 11/34 rats in Group 2 compared to 0/32 in Group 4 (p less than 0.0003). Early changes were examined by scanning and transmission electron microscopy as well as autoradiography. Preneoplastic liver foci were detected in infected groups of animals receiving amine and nitrate, indicating reabsorption of the carcinogen synthesized in situ to induce distant organ transformation. In another experiment, E. coli infection augmented bladder carcinogenesis by N-nitrosobutyl(4-hydroxybutyl)amine (NBHBA), as indicated by earlier appearance of bladder tumours (six weeks compared to nine weeks) and, after 25 weeks, higher incidences of transitional-cell carcinomas (41/46 compared to 39/53, p less than 0.05), squamous metaplasia (43% compared to 9%, p less than 0.0001), glandular metaplasia (26% compared to 13%, p less than 0.05) and muscle invasion (30% compared to 11%, p less than 0.01) in the E. coli-infected group receiving carcinogen compared to the noninfected group receiving carcinogen, respectively. These results indicate that bacterial infection of the urinary bladder may play a major role in bladder carcinogenesis, both by helping in-situ nitrosamine synthesis and by augmenting carcinogenesis by nitrosamines.

Amines↗
PubMed1987

Some aspects of cytochrome P450-dependent denitrosation of N-nitrosamines.

The present paper deals with three aspects of cytochrome P450-dependent denitrosation of N-nitrosamines. (1) Nitrate was found in addition to nitrite as a metabolic product of the denitrosation reaction when N-nitrosamines were incubated with a microsomal system. This could also be shown when nitric oxide was added to the microsomes. (2) In order to determine the amount of denitrosation in vivo, the nitroso group of N-nitroso-N-methylaniline was labelled with the 15N isotope and administered to rats; then, the concentrations of 15N-nitrate and 15-N-nitrite in the urine were quantified by measuring the reaction of nitrate and benzene to nitrobenzene. It is estimated from these data that about 33% of the applied dose of 15N-nitroso-N-methylaniline is denitrosated in vivo. (3) Although N-nitrosodiphenylamine (NDPhA) has been classified as a noncarcinogen, recent long-term and short-term studies have cast some doubt. In order to evaluate the mechanism by which NDPhA exerts its possible genetoxic effects, its metabolism was studied in vitro, and NDPhA and its metabolites were tested for induction of DNA single-strand breaks in rat hepatocytes and in Chinese hamster V79 cells. One metabolite was identified as diphenylamine; others were suspected to be the 4-hydroxylated derivative and its corresponding quinoneimine. NDPhA caused DNA damage in rat hepatocytes but not in V79 cells. Diphenylamine also gave negative results in V79 cells, but its putative metabolite, diphenylhydroxylamine, induced a significant increase in DNA single-strand breaks.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Different effects of chemicals on metabolism of N-nitrosamines in rat liver.

The effects of phenobarbital (PB), 3-methylcholanthrene (MC), pyrazole (PY) and ethanol (EtOH) pretreatment on N-nitrosodimethylamine (NDMA), N-nitrosobutylmethylamine (NBMA) and N-nitrosomethylbenzylamine (NMBzA) metabolism were examined in rats. In isolated hepatocytes, PB increased the metabolic decomposition of NBMA and NMBzA, and MC increased that of NBMA; PY and EtOH increased only that of NDMA. In studies of hepatic microsomal dealkylation, PB increased NBMA debutylation and NMBzA debenzylation, and MC increased NBMA debutylation; PY and EtOH increased NDMA demethylation selectively. Several cytochrome P450 (P450) species were active in dealkylating nitrosamines, indicating that the organ-specific carcinogenicity of nitrosamines might be changed by various P450 inducers.

Animals↗
PubMed1987

Effect of the trichothecene mycotoxin diacetoxyscirpenol on nitrosamine-induced oesophageal cancer and on relevant enzymes in oesophagus and liver.

To test the concept that human oesophageal cancer is initiated by nitrosamines and potentiated by consumption of food contaminated by mycotoxins produced by Fusaria, the effect of the trichothecene mycotoxin diacetoxyscirpenol (DS), alone and in combination with N-nitroso-N-methylbenzylamine (NMBzA), on rat oesophagus was studied. Chronic treatment with DS induced oesophageal hyperplasia, but simultaneous treatment with NMBzA tended to inhibit rather than to enhance carcinogenesis. The mycotoxin did not inhibit O6-alkylguanine-DNA alkyltransferase in oesophagus and produced a marked induction of repair protein in liver. Depletion of the repair protein in oesophagus brought about by injection of NMBzA was not inhibited by the mycotoxin, and its reappearance was not delayed. Intubation of DS reduced DNA synthesis in the oesophagus, while dietary treatment resulted in an increase after nine weeks. The results suggest that, while simultaneous treatment with DS reduces cancer induced by NMBzA, if there is first exposure to mycotoxin and induction of hyperplasia, and then exposure to nitrosamine, so that the carcinogen acts on a vulnerable oesophagus in which there is an increased rate of cell proliferation, the mycotoxin could well enhance carcinogenesis.

Animals↗
PubMed1987

Occurrence of volatile nitrosamines in food samples collected in three high-risk areas for nasopharyngeal carcinoma.

Fifty-four samples of foods consumed frequently in Tunisia, southern China and Greenland, all high-risk areas for nasopharyngeal carcinoma (NPC), were analysed for the presence of volatile nitrosamines by gas chromatography (GC) combined with a thermal energy analyser (TEA). Relatively high levels of N-nitrosodimethylamine (NDMA), N-nitrosopiperidine (NPIP) and N-nitrosopyrrolidine (NPYR) were found in Tunisian stewing base (touklia) and dried mutton preserved in olive oil (qaddid). In one Chinese salted and dried fish sample, a high level of NDMA (133 micrograms/kg) was detected, but for the 14 others the levels ranged from undetectable to 14 micrograms/kg, with a mean of 3 micrograms/kg. Similarly high levels of NDMA, were found in Eskimo dried, unsalted fish samples. NDMA, NPIP and NPYR at various levels were present in Chinese vegetables fermented in brine. The possible role of nitrosamines in the etiology of NPC is discussed.

China↗
PubMed1987

Effects of air-curing environment on alkaloid-derived nitrosamines in burley tobacco.

Levels of nitrite and pyridine alkaloid-derived total tobacco-specific nitrosamines (TSNA) were significantly higher in tobacco leaf (normal or late harvest) air-cured at 32 degrees C/83% relative humidity (RH) than in more moderate environments, i.e., 15 degrees C/50% RH and 24 degrees C/70% RH. These constituents increased appreciably from day 10 to day 21 of the cure. The near-concurrent appearances of maximal total contents of TSNA [sum of N'-nitrosonornicotine (NNN), N'-nitrosoanatabine (NAT), N'-nitrosoanabasine (NAB) and 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone) (NNK)] and nitrite supports the concept that nitrite is a limiting and proximal precursor of total TSNA during the curing of tobacco. During a long curing period (50 days) at 32 degrees C/83% RH, nicotine and anatabine contents decreased, but TSNA contents increased in leaves of all harvest dates and stalk positions. These results support the view that nicotine and anatabine are precursors of TSNA. Measurement of nitrite and individual alkaloids during post-harvest processing of tobacco leaf may provide an index of the potential accumulation of alkaloid-derived nitrosamines.

Agriculture↗
PubMed1987

Determination of N-nitrosamines in gastric juice and urine and a comparison of endogenous formation of N-nitrosoproline and its inhibition in subjects from high- and low-risk areas for oesophageal cancer.

Samples of gastric juice were collected from a high-risk area for oesophageal cancer in China and analysed for N-nitroso compounds. N-Nitrosodimethylamine (NDMA), N-nitrosodiethylamine (NDEA), N-nitrosomethylbenzylamine (NMBzA), N-nitrosopyrrolidine (NPYR) and N-nitrosopiperidine (NPIP) were identified in descending order of concentration. Several unknown compounds were also detected in the fasting gastric juice. A positive correlation was found between the amount of nitrosamines in gastric juice and the degree of severity of lesions of the oesophageal epithelium: the amounts of nitrosamines in gastric juice from subjects with a normal oesophageal epithelium were lower than those in subjects with marked dysplasia or carcinoma of the oesophagus. In addition, 1500 samples of 24-h urine were collected from various communes in six high-risk areas and two low-risk areas for this cancer in China and analysed for N-nitrosamino acids. Subjects in high-risk areas excreted higher levels than those in low-risk areas. Intake of L-proline resulted in marked increases in levels of urinary N-nitrosoproline (NPRO) in inhabitants from both high- and low-risk areas. Intake of moderate doses of vitamin C, alpha-tocopherol and zinc by high-risk subjects reduced the urinary levels of N-nitrosamino acids to those found in undosed subjects in low-risk areas, suggesting a rational basis for prevention in high-risk areas.

China↗
PubMed1986

Induction of oral cavity tumors in F344 rats by tobacco-specific nitrosamines and snuff.

The tumorigenic activities toward the oral cavity of snuff, its extracts, and two of its major nitrosamines, N'-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were evaluated in male F344 rats. In one protocol, groups of 21-30 rats were treated beginning at age 10 weeks by chronic application to the oral cavity for 131 weeks of either H2O, an H2O extract of snuff, an H2O extract of snuff enriched with ten times its indigenous concentration of NNN and NNK, or with NNN and NNK in H2O. The incidence of oral cavity tumors in the rats treated with NNN and NNK was 8 of 30, compared to 0 of 30 in controls (P less than 0.05). These results demonstrate that NNN and NNK can induce tumors locally in the oral cavity of F344 rats. Oral cavity tumors were also observed in 3 of 30 rats treated with snuff extract enriched with NNN and NNK, but not in the rats treated with snuff extract alone. In a second protocol, a test canal was surgically created in the lower lip of groups of 21-32 rats, and either snuff, H2O-extracted snuff, or snuff enriched with its own H2O extract was inserted in the test canal 5 times weekly for 116 weeks. A group of 10 control rats had surgery only. Among the 32 rats treated with snuff, 3 had oral cavity tumors; one was a squamous cell carcinoma originating in the test canal and invading the gingiva, one was a papilloma of the test canal, and one was a papilloma of the hard palate. Oral cavity tumors were also observed in 2 of 21 rats treated with H2O-extracted snuff and 1 of 32 rats treated with snuff enriched with its H2O extract. Oral tumors were not observed in control rats. The results of this study indicate that snuff and individual nitrosamines present in snuff can induce oral cavity tumors in F344 rats and support the epidemiological observations which indicate that snuff dipping causes oral cancer in man.

Animals↗
PubMed1986

Increase in human exposure to methylamine precursors of N-nitrosamines after eating fish.

Consumption of fish has been encouraged recently because it may prevent mortality due to heart disease. Fish contains methylamines, which are precursors of N-nitrosamines. Nitrosamines can act as potent carcinogens in a wide variety of animal species, and there is no reason to assume that humans are resistant. Human subjects (n = 5) ingested a diet of known methylamine content for 2 days. On Day 3, they ate fish at the luncheon and dinner meals. On Day 4, they again ate the control diet. A single portion of fish contained as many methylamines as were normally excreted by the human in 2 days. Urinary excretion of monomethylamine remained constant (1.3 to 1.5 mumol/24 h/kg of body weight) throughout the study. Dimethylamine excretion increased more than 4-fold after fish was eaten (from 5.6 to 24.1 mumol/24 h/kg of body weight), while trimethylamine excretion increased more than 8-fold (from 0.2 to 1.6 mumol/24 h/kg of body weight). We conclude that the consumption of fish significantly increased exposure to methylamines, particularly to dimethylamine. Although there is potential for the in vivo conversion of dimethylamine to nitrosodimethylamine, a carcinogen, we know of no studies that have determined that the ingestion of fish increases the risk of cancer. This should be carefully investigated prior to recommending that humans change their eating habits.

Adult↗
PubMedDate not supplied

Current trends in levels of volatile N-nitrosamines in fried bacon and fried-out bacon fat.

Commercially processed bacon samples purchased from the Washington, DC, retail market have been periodically analyzed since 1971 for the presence of volatile N-nitrosamines in the fried product. During that time, a downward trend in the concentration of N-nitrosopyrrolidine has been observed, and between 1978 and 1980 it plateaued at 4-30 ppb, with an average of 11 ppb. A recent survey, however, indicates a change in this downward trend, with N-nitrosopyrrolidine found at levels ranging from 1 to 65 ppb, average 21 ppb. Volatile N-nitrosamines were found at levels up to 110 ppb in the fried product and up to 85 ppb in the fried-out bacon fat.

Animals↗
PubMed1985

Rapid assay of N-butyl-N-(3-carboxypropyl)nitrosamine in rat organs and urine by high-performance liquid chromatography after derivatization.

The concentration of N-butyl-N-(3-carboxypropyl)nitrosamine (BCPN), which is the major metabolite of the carcinogen N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), was measured in the urine, thymus, liver, kidney, and bladder of rats orally administered with BBN. Since BCPN is a carboxylic acid, it forms an ester with 9-anthryldiazomethane (ADAM), which is a fluorescent labeling agent highly sensitive to carboxylic acids. Thus, BCPN and ADAM were reacted at 40 degrees for 1 hr, and the resulting ester was separated and measured by high-performance liquid chromatography (HPLC) with a reverse-phase type column. The range of measurement was 0 to 40 micrograms/ml, and the coefficient of variation (CV) was 3.8%. When 0.025% BBN was given orally to rats in tap water, the BCPN concentration in the urine was very high at 220 micrograms/ml, while it was 0.15 microgram/100 mg in the wet tissues of the thymus, 0.35 microgram/100 mg in the liver, 0.40 microgram/100 mg in the kidney, and 1.2 microgram/100 mg in the bladder. The BCPN concentration in the bladder, in which tumors are induced by the administration of BBN, was thus higher than those in the other organs.

Animals↗
PubMed1985

Effects of riboflavin deficiency on metabolism of nitrosamines by rat liver microsomes.

The effects of riboflavin deficiency on the metabolism of N-nitrosodimethylamine [(DMN) CAS: 62-75-9] and other nitrosamines were examined in rats. After weanling rats were put on a riboflavin-deficient diet, the development of the deficiency was monitored by the growth rate and the erythrocyte glutathione reductase activation coefficient. In the riboflavin-deficient rats, the liver microsomal NADPH-cytochrome c reductase activity was lower but the cytochrome P450 content was higher than that of the control. The metabolism of DMN was dependent on the severity of the deficiency. During mild deficiency, which was observed mainly with Sprague-Dawley rats, the microsomal DMN demethylase (DMNd) activity was elevated 30-80%, but the metabolism of N-nitrosomethylbenzylamine (CAS: 937-40-6) and three other nitrosamines was slightly decreased. Dietary restriction in the pair-fed group also caused an elevation of DMNd activity above that of the ad libitum control group due to a partial fasting effect. During severe deficiency, which was observed mainly with Wistar rats, however, the metabolism of DMN, as well as the oxidation of benzo[a]pyrene, was decreased. Preincubation with flavin adenine dinucleotide and flavin mononucleotide enhanced the DMNd activity of the microsomes from riboflavin-deficient rats but not that from control rats. The results suggest that, depending on the alterations of the monooxygenase enzyme system during the development of the deficiency, riboflavin deficiencies may have different effects on the metabolism of DMN and some other carcinogens.

Animals↗
PubMed1979

Agglutination of bladder cells by concanavalin A during the early phase of treatment of rats with N-butyl-N-(4-hydroxybutyl)nitrosamine.

N-Butyl-N-(4-hydroxybutyl)nitrosamine was given to male Wistar rats at a dose of 0.05% in the drinking water for one to five weeks, and agglutination of cell isolated from their bladder by concanavalin A (Con A) was determined at intervals during and after treatment. Mucosal cells were isolated from everted bladder by ethylenediaminetetraacetate treatment and sonication. As early as one week after the start of treatment, Con A caused some agglutination of isolated bladder cells, and this agglutination increased with time, reaching an almost constant value from the third week. Con A agglutination of bladder cells induced by N-butyl-N-(4-hydroxybutyl)nitrosamine treatment for only one week appeared to be irreversible, and it was still observed two weeks after the end of treatment. Scanning electron microscopy showed that microvilli developed on the luminal surface of mucosal cells in situ at the time when the isolated cells became agglutinable with Con A. Measurement of agglutinability of isolated bladder cells with Con A might be a useful way of detecting very early changes in bladder carcinogenesis.

Agglutination↗
PubMed1979

Intake of volatile nitrosamines from consumption of alcohols.

Volatile nitrosamines were determined in alcoholic drinks during epidemiologic studies on the relationship between esophageal cancer incidence and alcohol consumption in Normandy, France. Nitrosodimethylamine (NDMA) was found commonly in most alcoholic drinks tested, with the exception of wine. The average level, about 2 micrograms/liter in beers, was higher than that for other drinks; the range was 0.2--8.6 micrograms/liter. Traces of nitrosodiethylamine (NDEA) were also detected in spirits and ciders. No significant increases in levels were found after nitrosation. Calculation of daily intake in the study region showed that the main intake of volatile nitrosamine is from NDMA in beer. The intake of NDEA through consumption of cider is about one-third that of NDMA from all sources.

Alcoholic Beverages↗
PubMed1977

Survey of finfish and shellfish for volatile N-nitrosamines.

A variety of finfish and shellfish obtained on the local retail market were analyzed for 14 volatile N-nitrosamines by using a gas-liquid chromatographic method demonstrated to be sensitive to 10 ppb (microng/kg). A total of 78 samples (fresh, frozen, and canned), representing 26 varieties of fish, were analyzed. No nitrosamines were found.

Animals↗
PubMed1978

Survey of cured meat products for volatile N-nitrosamines: comparison of two analytical methods.

A survey of 106 cured meat samples for 14 volatile N-nitrosamines has been completed. N-Nitrosopyrrolidine has been confirmed in fried bacon at levels ranging from 5 to 75 ppb. Unconfirmed trace levels of N-nitrosodimethylamine have been observed in a variety of cured meat products. The comparison of the multidetection GLC-MS method with the mineral oil distillation TEA method for the determination of volatile N-nitrosamines in foods shows good agreement between the analytical methods, especially at the 10 ppb level, and excellent agreement between the GLC and TEA analyses of an identical sample extract.

Animals↗
PubMed1984

[Determination by capillary gas liquid chromatography of nitrosamine in partially altered food].

The nitrosamines have been extensively studied for their toxicity. Their formation in the foods containing nitrous and nitric derivatives is favoured by the presence of suitable substrata. In the present work have been used column and capillari GL Chromatography for the determination of some nitrosamines in altered foods. The results obtained by applying the suggested procedure to a number of altered samples have been very encouraging.

Chromatography, Gas↗
PubMed1984

Comparative metabolism of beta-oxidized nitrosamines.

Several beta-oxidized nitrosamines have been shown to induce pancreatic cancer in Syrian hamsters. N-Nitrosobis(2-oxopropyl)amine (ND2OPA) is the most specific, but it also induces either colonic or prostatic tumours in MRC-Wistar rats. In-vivo and in-vitro metabolic studies show that N-nitrosomethyl(2-oxopropyl)amine is a metabolite of ND2OPA in hamsters but not in rats. ND2OPA is also present in higher concentrations in hamster pancreas than in the liver. No similar effect occurs in rats. These factors may explain, in part, the organotropism and species specificity of this nitrosamine.

Animals↗