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PubMed2006

Variability in fecal water genotoxicity, determined using the Comet assay, is independent of endogenous N-nitroso compound formation attributed to red meat consumption.

Red meat consumption causes a dose-dependent increase in fecal apparent total N-nitroso compounds (ATNC). The genotoxic effects of these ATNCs were investigated using two different Comet assay protocols to determine the genotoxicity of fecal water samples. Fecal water samples were obtained from two studies of a total of 21 individuals fed diets containing different amounts of red meat, protein, heme, and iron. The first protocol incubated the samples with HT-29 cells for 5 min at 4 degrees C, whereas the second protocol used a longer exposure time of 30 min and a higher incubation temperature of 37 degrees C. DNA strand breaks were quantified by the tail moment (DNA in the comet tail multiplied by the comet tail length). The results of the two Comet assay protocols were significantly correlated (r = 0.35, P = 0.003), however, only the second protocol resulted in detectable levels of DNA damage. Inter-individual effects were variable and there was no effect on fecal water genotoxicity by diet (P > 0.20), mean transit time (P = 0.588), or weight (P = 0.705). However, there was a highly significant effect of age (P = 0.019). There was no significant correlation between concentrations of ATNCs in fecal homogenates and fecal water genotoxicity (r = 0.04, P = 0.74). ATNC levels were lower in fecal water samples (272 microg/kg) compared to that of fecal homogenate samples (895 microg/kg) (P < 0.0001). Failure to find dietary effects on fecal water genotoxicity may therefore be attributed to individual variability and low levels of ATNCs in fecal water samples.

Ammonia↗
PubMed2002

Diels-Alder and ene reactions of singlet oxygen, nitroso compounds and triazolinediones: transition states and mechanisms from contemporary theory.

Singlet oxygen, nitroso compounds and triazolinediones have similar electronic structures: they share a low lying LUMO, making them powerful electrophiles, and a high lying HOMO, orthogonal to the LUMO and consisting of an antibonding combination of lone paris. This bestows some nucleophilic character on these species. We describe a number of studies employing the best levels of theory currently available for systems of this size and demonstrate that the Diels-Alder and ene reactions of these three species are calculated to show subtle changes in mechanism. The calculations have been calibrated, wherever possible, by comparison to experimental observations including measured activation and reaction energies, regio- and stereo-selectivities, intermediates observed either spectroscopically or by trapping, and kinetic isotope effects.

Journal Article↗
PubMedDate not supplied

An investigation of the levels of N-nitrosodimethylamine, apparent total N-nitroso compounds and nitrate in beer.

Over 170 retail samples of beer have been analysed for N-nitrosodimethylamine (NDMA), apparent total N-nitroso compounds (ATNC) and nitrate. Levels of NDMA ranged from below 0.1 up to 1.2 micrograms/kg with a mean of 0.2 micrograms/kg. ATNC was detected in 42% of the samples in concentrations of up to 569 micrograms (N-NO)/kg. The levels of nitrate ranged from less than 0.2 up to 143 mg/kg with a mean of 16.8 mg/kg. There was no correlation between the amounts of NDMA and ATNC found in the retail beers. Samples taken during the course of fermentation showed that NDMA was unaffected by the bacterial reduction of nitrate which causes ATNC formation. HPLC studies using a photolysis/chemiluminescence detector revealed that the ATNC in beer are highly polar species of as yet unknown identity.

Beer↗
PubMed1993

Method for group determination of total N-nitroso compounds and nitrite in fresh gastric juice by chemical denitrosation and thermal energy analysis.

A method for the determination of total N-nitroso compounds (NOC) and nitrite in fresh human gastric juice is described, which is based on earlier methods. A freshly obtained gastric juice sample is injected directly into refluxing ethyl acetate containing glacial acetic acid, HCl and HBr to determine the total concentration (A) of nitrite, total NOC and thermo- and acid-labile thermal energy analyser (TEA)-responsive compounds (TAC). Another fresh sample of the same juice (with or without the addition of sulfamic acid) is injected directly into refluxing ethyl acetate containing glacial acetic acid and HCl for determining the TAC level (B) and the total level (C) of nitrite and TAC. The NO released from nitrite, TAC and NOC is detected by TEA acting as a chemiluminescence detector. The differences between A and C and between C and B represent the concentrations of total NOC and nitrite, respectively. The method is rapid, reproducible (relative standard deviation 1-6%) and sensitive (detection limit 1.0 pmol). The behaviour of nitrite and NOC in the analytical system was studied and relevant techniques for the direct analysis of fresh gastric juice samples and for stabilization of fresh samples have been developed.

Differential Thermal Analysis↗
PubMed1983

N-nitroso compounds: evidence for their presence in airborne particles.

Chemical, infrared, and thermal energy analyses have provided evidence for the presence of the N-nitroso functional group in extracts of airborne particles. The total molar N-nitroso concentrations in New York City air are equivalent to the total concentrations of polycyclic aromatic hydrocarbons. Since 90 percent of the N-nitroso compounds that have been tested are carcinogens, the newly discovered but untested materials may represent a significant environmental hazard.

Air Pollutants↗
PubMedDate not supplied

N-nitroso compounds and Helicobacter pylori in the gastric remnant.

AIMS AND BACKGROUND: The aims of this study were to investigate the role of N-nitroso compounds (NOC) and Helicobacter pylori (H. pylori) in gastric stump carcinogenesis. METHODS AND STUDY DESIGN: Analyses of biochemical parameters such as pH and NOC concentration were carried out on 65 fasting gastric juice samples obtained at endoscopy from 45 patients previously submitted to partial gastrectomy for benign peptic ulcer disease (23 Billroth I, 22 Billroth II/Reichel-Polya) and 20 normal controls. Biopsy specimens were taken to determine histology and H. pylori status. RESULTS: Significantly higher mean pH values and NOC concentrations were found in partial gastrectomies compared to normal controls. In relation to surgical methods, higher mean pH values and NOC concentrations were observed in the gastric juice of patients with Billroth II compared to Billroth I gastrectomies. Independently of the type of surgical reconstruction, higher mean NOC levels were recorded in patients with more severe histological changes and H. pylori infection. CONCLUSIONS: All these data suggest that high levels of NOC in gastric juice and H. pylori infection could be cofactors in gastric stump carcinogenesis.

Adult↗
PubMed1994

Dietary garlic suppresses DNA adducts caused by N-nitroso compounds.

The present studies examined the impact of a processed garlic powder on the in vivo occurrence of DNA adducts caused by N-nitroso compounds (NOC) in rats. Addition of 2% garlic powder to diets containing aminopyrine and sodium nitrite (each at 600 mg/kg) reduced the occurrence of both 7-N-methyldeoxyguanosine (7-N-mG) and 6-O-methyldeoxyguanosine (6-O-mG) adducts to rat liver DNA by approximately 55%; and over 80% when 4% garlic was provided. Dietary supplementation with garlic powder (2 and 4%) also reduced the occurrence of 7-N-mG and 6-O-mG adducts by approximately 40 and 60% respectively, in rats intubated with N-nitrosodimethylamine (150 mg/kg body wt). The quantity of 7-N-mG and 6-O-mG adducts in mammary tissue of rats given intravenous N-methyl-N-nitrosourea (50 mg/kg body wt) was reduced over 50% in rats fed 2% garlic compared to controls. The depression in the occurrence of these adducts was approximately 70% when dietary garlic was increased to 4%. These experiments suggest the reduction in DNA adducts caused by processed garlic powder likely reflects a depression in the formation of NOC from precursors and changes in the bioactivation and/or denitrosation of NOC.

Animals↗
PubMed2007

N-Nitroso compounds produced in deer mouse (Peromyscus maniculatus) GI tracts following hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) exposure.

Given the potent carcinogenic effects of most N-nitroso compounds, the reductive transformation of the common explosive hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) to a group of N-nitroso derivatives, hexahydro-1-nitroso-3,5-dinitro-1,3,5-triazine (MNX), hexahydro-1,3-dinitroso-5-nitro-1,3,5-triazine (DNX), and hexahydro-1,3,5-trinitroso-1,3,5-triazine (TNX) in the environment have caused concerns among the general public. Questions are arising about whether the same transformations also occur in mammals, and if true, to what extent. This study investigated the N-nitroso derivatives production in the deer mouse GI tract following RDX administration. Findings verified that such transformations do occur in the mammalian GI tract at notable levels: the average MNX concentrations in deer mice stomach were 85 microg/kg and 1318 microg/kg for exposure to 10mg/kg and 100mg/kg diet, respectively. DNX in stomach were 217 microg/kg for the 10mg/kg dose group and 498 microg/kg for the 100mg/kg dose group. Changes in other toxic endpoints including body weight gain, food consumption, organ weight, and behavior were also reported.

Animals↗
PubMed2003

N-nitroso compounds in the gastrointestinal tract of rats and in the feces of mice with induced colitis or fed hot dogs or beef.

Because colonic N-nitroso compounds (NOC) may be a cause of colon cancer, we determined total NOC levels by Walters' method in the gastrointestinal tract and feces of rodents: (i) feces of C57BL mice fed chow and semi-purified diets contained 3.2 +/- 0.4 and 0.46 +/- 0.06 NOC/g, respectively (P < 0.01, mean +/- SD). (ii) NOC levels for gastrointestinal contents of three groups of Sprague-Dawley rats fed chow diet were 0.9 +/- 0.05 (diet), 0.2 +/- 0 (stomach), 0.3-0.4 (small intestine), 0.7-1.6 (cecum and colon) and 2.6 +/- 0.6 (feces) nmol/g. NOC precursor (NOCP) levels (measured as NOC after mild nitrosation) for two rat groups fed chow diet showed a 16-fold increase from stomach to proximal small intestine (mean, 6.2 micromol/g), and a 1.7-fold increase from distal colon to feces (mean, 11.6 micromol/g). (iii) Eight Min and five C57BL/6J mice received 4% dextran sulfate sodium in drinking water on days 1-4 to induce acute colitis. This increased fecal NOC levels 1.9-fold on day 5 in both strains (P < or = 0.04), probably due to NO synthase-derived nitrosating agents in the colon. (iv) Following studies on humans fed beef [Hughes et al. (2001) Carcinogenesis, 22, 199], Swiss mice received semi-purified diets mixed with 18% of beef plus pork hot dogs or sautéed beef for 7 days. On day 7, individual 24-h fecal NOC outputs were determined. In three hot dog and two beef groups with 5 mice/group, mean fecal NOC output/day was 3.7-5.0 (hot dog) and 2.0-2.9 (beef) times that for control groups fed semi-purified diet alone (P < 0.002 for each of combined groups). These groups showed little change in fecal NOCP output. (v) Initial purification of rat fecal NOCP by adsorption-desorption and HPLC is described. Results should help evaluate the view that colonic NOC causes colon cancer associated with colitis and ingestion of red and nitrite-preserved meat.

Animals↗
PubMed1998

Studies of initiation and promotion of carcinogenesis by N-nitroso compounds.

Complete carcinogens must possess both initiating and promoting properties. Most N-nitroso compounds are mutagens and are considered to be initiators, but some are not mutagenic and yet are complete carcinogens. To investigate the two activities, brief treatments of male F344 rats with each of three mutagens, nitrosodimethylurea, nitrosodiethylurea and nitrosobis-(2-oxopropyl)-amine, were followed by chronic treatment (40 weeks) with one of four non-mutagens, nitrosomethyl-3-carboxypropylamine, nitrosodiethanolamine, nitrosomethyl-2-hydroxypropylamine or phenobarbital, the last being a well-known promotor of liver tumors in rats. Each treatment group consisted of 18 animals and there were control groups of 15 animals without initiation and 15 animals without promotion. All surviving rats were sacrificed at week 78. There were almost no tumors in untreated controls or in groups treated with the promotors, other than bladder tumors in one group. Certain tumors were numerous in the initiated groups, but there were only a few instances of increased incidences after treatment with the promotors. The action of the initiators appeared to be the dominant factor and there was scant indication in this experiment of the induction of tumors by the promotors of promotion of initiated cells in most organs (e.g. the liver). This indicates that it is unlikely that non-genotoxic carcinogens induce tumors by promotion of already-initiated cells, but that some other mechanism prevails.

Animals↗
PubMed1990

[Effects of vitamin A on the activity of glutathione system enzymes of liver detoxication after administration of nitroso-compound precursors to rats].

The activity of glutathione system enzymes exposed to nitroso-compound (NC) precursors in small doses for 12 months and preliminary injection of vitamin A have been studied. The histo- and biochemical examinations have revealed a pronounced increase in the enzyme activity exposed of NC precursors and a slight increase when injecting preliminary vitamin A.

Animals↗
PubMed1989

Photolytic interface for high-performance liquid chromatography--chemiluminescence detection of non-volatile N-nitroso compounds.

A photolytic interface between high-performance liquid chromatography (HPLC) and a chemiluminescence detector has been developed for the trace detection of non-volatile N-nitroso compounds in biological matrices. A chromatographic effluent containing separated N-nitrosoamino acids and N-nitrosamides is introduced into a glass coil with a purge stream of He and irradiated with ultraviolet light. Nitrogen oxide, cleaved by photolysis, is separated rapidly from the solvent through a series of cold traps and carried by the He into the reaction chamber of a chemiluminescence detector. The method is compatible with most types of HPLC, especially reversed-phase, and yields low-nanogram sensitivity for underivatised N-nitrosoamino acids and N-nitrosamides. The detection of a model N-nitrosamide, trimethylnitrosourea, in spiked porcine gastric fluid (42 micrograms l-1), and of N-nitrosoproline and N-nitroso-1,3-thiazolidine-4-carboxylic acid, in spiked human urine (7-8 micrograms l-1), is demonstrated.

Animals↗
PubMed1984

Genetic and biochemical factors affecting the induction of bacteriophage lambda by N-nitroso compounds.

As part of our effort to validate a biochemical (prophage) induction assay (BIA) as a screening test for carcinogens, we have tested more than 100 N-nitroso compounds. An enzyme, beta-galactosidase, is induced as an indirect consequence of DNA damage to the host, as part of the 'SOS' response. Besides the obvious practical importance of detecting this class of carcinogen, there is the question of the mechanism by which these compounds work. Mutagenesis by one compound, N-methyl-N'-nitro-N-nitrosoguanidine, is known to proceed by both SOS (recA)-dependent and SOS-independent pathways. Mispairing due to O6 alkylation of guanine is thought to be responsible for the SOS-independent pathway; however, there has been little consideration of recA-dependent functions, of which phage induction is one. Although nitrosamides could be detected as phage inducers in our assay, N-nitrosamines in the presence of rat liver 9 000 X g supernatant usually gave no response. We found that the use of several mutant strains, particularly a lexA mutant, in combination with hamster liver 9 000 X g supernatant, allowed us to detect most N-nitrosamines reasonably well, in either a spot test or a quantitative tube assay. Induction in a lexA strain was most unexpected, since this mutation usually diminishes the expression of SOS functions induced by ultra-violet light. Because the genetic and biochemical conditions that favour phage induction are different from those that favour mutagenesis, it seems likely that the lesions in DNA leading to the two biological end-points are different.

Bacteriophage lambda↗
PubMed1993

Instability of N-nitroso compounds in gastric juice and preliminary results from analyses of fresh samples by using an improved analytical method.

Using an improved method for determination of total N-nitroso compounds (NOC), we examined the stability of those compounds in fresh gastric juice samples during storage and the effects of the addition of 2% sulphamic acid on NOC concentration in 212 samples. The NOC levels in fresh samples decreased very rapidly at -20 degrees C, especially during the first 24 hours of storage (P < 0.01), and nitrite concentration also showed a decreasing trend during storage. The addition of sulphamic acid significantly reduced NOC levels from 1.97 +/- 0.21 to 1.10 +/- 0.12 mumol/l (mean +/- SE, P < 0.01), especially in samples of initially high pH. However, in some individual samples (16.5%) the NOC levels actually increased by 14.1% (P < 0.01). The results from analysis of NOC in 212 fresh samples in relation to pH demonstrated two significantly higher peaks of NOC concentrations at intragastric pH ranges 1.1 to 2.99 (P < 0.05) and 6.0 to 7.9 (P < 0.01). There was a significant relationship between nitrite level and intragastric pH (r = 0.480, P < 0.01), the nitrite concentration increasing dramatically when the pH exceeded 6.0. The present study suggest that a major proportion of the unidentified NOC formed through intragastric nitrosation is labile NOC; if the true concentration of NOC is to be determined it is therefore essential to analyse fresh gastric juice samples directly after collection and without pretreatment. It will also be necessary to characterize those labile NOC in order to study further the mechanism of endogenous N-nitrosation in man and its relation to human carcinogenesis.

Gastric Juice↗
PubMed2002

Dietary exposure and urinary excretion of total N-nitroso compounds, nitrosamino acids and volatile nitrosamine in inhabitants of high- and low-risk areas for esophageal cancer in southern China.

We assessed the exposure of total N-nitroso compounds (TNOCs) in the inhabitants of high- and low-risk areas for esophageal cancer in southern China. Samples of 24 hr diet and 12 hr overnight urine were collected from 120 male adults in each of the 2 areas, a high-risk area (Nan'ao County) and a low-risk area (Lufeng County) for esophageal cancer. Annual standardized mortality rates of esophageal cancer in Nan'ao and Lufeng are 110/10(6) and 10/10(6) respectively. The 240 healthy male subjects (35-64 years old) were selected by a 3-stage random cluster sample procedure. Levels of TNOCs, NAAs and volatile nitrosamines in the samples were measured. The TNOC detection rate (95%) in the diet, the TNOC daily intake (4.25 +/- 0.84 micromol), TNOC excretion levels (0.04 +/- 0.01 nmol/12 hr) and daily intake of volatile nitrosamines (5.84 +/- 0.71 micromol) in the high-risk area were significantly greater than values in the low-risk area (A +/- B = mean +/- SE). The TNOC detection rate in the diet, the TNOC daily intake, TNOC excretion levels and daily intake of volatile nitrosamines in the low-risk area were 70%, 0.25 +/- 0.06 micromol, 0.02 +/- 0.01 nmol/12 hr and 3.18 +/- 0.31 micromol, respectively. NAA excretion levels showed no difference between the 2 areas (16.3 +/- 7.18 micromol/12 hr for Nan'ao and 31.2 +/- 26.4 micromol/12 hr for Lufeng). Thus, TNOCs are implicated in the etiology of esophageal cancer in southern China.

Adult↗
PubMed1991

N-nitroso compounds, genotoxins and their precursors in gastric juice from humans with and without precancerous lesions of the stomach.

We are investigating the interrelationships between levels of total N-nitroso compounds (NOC), genotoxic activity (both before and after nitrosation), degree of bacterial colonization in gastric juice and degree of severity or absence of precancerous lesions of the stomach. The mean level of constitutive total NOC in gastric juice was similar in the different groups of patients, but it was higher in acidic gastric juice (n = 30) than in gastric juice at pH greater than 4.5 (n = 12). Acid-catalysed nitrosation of gastric juice in vitro increased the concentration of total NOC by up to several thousand fold, to a maximum of 1330 mumol/l. Genotoxicity, expressed as SOS-inducing potency per 100 microliters of gastric juice was measurable in only 20% of gastric juice samples tested. After acid-catalysed nitrosation, however, all samples showed genotoxic activity, the mean SOS-inducing potency being four to seven times greater than the corresponding constitutive value. There was no association between the mean SOS-inducing potency of gastric juice and the severity of precancerous lesions. The mean SOS-inducing potency of neutral or basic gastric juice was slightly greater than that of acidic samples. In a kinetic study on N-nitrosation of gastric juice in vitro, a mixture of amino and amido substrates was nitrosated; both qualitative and quantitative individual differences in nitrosatable substrates in gastric juice were seen. Fractionation of acidic, neutral and basic nitrosated gastric juice samples revealed a preponderance of nonvolatile, unknown NOC with varying polarities. The results of our study suggest that only pH determines the nature and level of precursors of NOC and of nitrosation-dependent genotoxins in gastric juice.

Adult↗
PubMed1989

Human exposure to endogenous N-nitroso compounds: quantitative estimates in subjects at high risk for cancer of the oral cavity, oesophagus, stomach and urinary bladder.

A sensitive procedure to quantitate human exposure to endogenous N-nitroso compounds (NOC) has been developed. It is based on the excretion of N-nitrosoproline (NPRO) and other N-nitrosamino acids in the urine, which are measured as an index of endogenous nitrosation, following ingestion of precursors. The NPRO test has been applied to human subjects in clinical and epidemiological studies, and the kinetics and dietary modifiers of endogenous nitrosation have been investigated. Results obtained after application of the NPRO test to subjects at high risk for cancers of the stomach, oesophagus, oral cavity and urinary bladder are summarized. In most instances, higher exposures to endogenous NOC were found in high-risk subjects, but individual exposure was greatly affected by dietary modifiers or disease state. Vitamin C efficiently lowered the body burden of intragastrically formed NOC. The results point to an aetiological role of NOC in these human cancers and provide an interpretation of epidemiological findings that have shown protective effects of fruits and vegetables against several malignancies.

China↗