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PubMed1985

Studies in gastric carcinogenesis. II. Absence of elevated concentrations of N-nitroso compounds in the gastric juice of Greek hypochlorhydric individuals.

The concentrations of nitrate, nitrite, N-nitroso compounds and bacteria were measured in 96 samples of fasting gastric juice, pH 0.90-8.50, obtained from 56 individuals just before or at various times (8 days - 1 year) after gastric operation. The mean pH of the post-operative samples [4.66 +/- 0.39 (SEM)] was significantly higher than that of the pre-operative ones [3.29 +/- 0.33 (SEM)]. A positive correlation with pH was observed for the concentrations of total and nitrate-reducing bacteria (median values 5.0 X 10(5) organisms/ml and 9.2 X 10(4) organisms/ml, respectively, for samples with pH greater than or equal to 1.2 X 10(3) organisms/ml and 0 organisms/ml, respectively, for samples with pH less than or equal to 2.5) and nitrite [mean values 22.5 +/- 3.1 (SEM) microM and 3.20 +/- 0.5 (SEM) microM for samples with pH greater than or equal to 6.5 and pH less than or equal to 2.5, respectively]. No correlation with pH was seen for the concentrations of nitrate [mean value 0.48 +/- 0.06 (SEM) mM] or N-nitroso compounds [mean value 0.30 +/- 0.06 (SEM) microM]. The concentrations of bacteria and nitrite, although increased in hypochlorhydric individuals, were lower than those reported for corresponding individuals in other, primarily British, studies. It is suggested that the relatively low concentrations of nitrite observed in our hypochlorhydric population may account for the absence of elevated concentrations of N-nitroso compounds and that the latter phenomenon may be related to the relatively low frequency of gastric cancer in Greece.

Adult↗
PubMedDate not supplied

Carcinogenicity and mutagenicity of N-nitroso compounds.

The carcinogenic activities in rats and hamsters and the mutagenic activity in Salmonella of a number of N-nitroso compounds belonging to various classes have been compared. While most directly acting N-nitroso compounds and those requiring metabolic activation are mutagenic with appropriate activation and seem to alkylate DNA in vivo, there are exceptions. Some of these are mutagens that are not carcinogenic; others are carcinogens that are nonmutagenic. Even among the mutagenic carcinogens, there is no quantitative relationship between mutagenic and carcinogenic activities. This implies to directly acting compounds and to those requiring metabolic activation. The lack of congruence between the two activities among the nitrosamines is due to the complexity of the metabolic activating processes leading to formation of proximate carcinogens. The deficiencies in the mutagenesis assay appear to arise from a lack of the necessary enzymes in the liver microsomal fractions used for activation. Nitrosamines bearing oxygen on the beta carbon of an alkyl chain are not oxidized by rat microsomal enzymes and hence are not converted to bacterial mutagens by rat liver microsomes. Bacterial mutagenicity is not a guide to carcinogenic activity of N-nitroso compounds or to the mechanisms by which these compounds induce cancer.

Animals↗
PubMed1985

[Interaction of different N-nitroso compounds with DNA in vitro].

The interaction of 11 N-nitroso compounds of different structure and carcinogenic activity with DNA in vitro under the influence of UV light was studied by the method of melting. UV light is shown to induce the DNA damage by N-nitroso compounds irrespective of their carcinogenic activity.

DNA↗
PubMed1991

Endogenous N-nitrosation in man assessed by measurement of apparent total N-nitroso compounds in faeces.

The faecal concentration of substances responding to the chemical test for N-nitroso compounds (apparent total N-nitroso compounds, ATNC) was investigated in human subjects consuming their normal free-choice diet. Concentrations ranged from 40 to 590 micrograms (N-NO)/kg faeces. To ascertain the likely relative contributions of endogenous ATNC formation and preformed, dietary ATNC, the subjects consumed a diet low in nitrate and ATNC for 8 days. At the end of this period, ATNC had decreased substantially with concentrations ranging from below the 40 micrograms (N-NO)/kg detection limit up to 143 micrograms (N-NO)/kg, mean 82 micrograms (N-NO)/kg. On supplementing this diet with 300 mg nitrate/day, faecal ATNC levels increased markedly. On the third day of this regime, values were in the range 73-714 micrograms (N-NO)/kg with a mean of 307 micrograms (N-NO)/kg. The results, together with the known limited occurrence of ATNC in the majority of foodstuffs so far tested, generally non-detectable or less than 100 micrograms (N-NO)/kg, suggest that endogenous formation via species derived from dietary nitrate is likely to be an important source of ATNC in human faeces.

Adult↗
PubMed1982

Formation of nitroso compounds and mutagens from cinnarizine, ethambutol, piromidic acid, pyridinol carbamate and tiaramide by drug/nitrite interaction.

The formation of nitroso compounds and mutagens from 5 nitrogen-containing drugs (cinnarizine, ethambutol, piromidic acid, pyridinol carbamate and tiaramide) by drug/nitrite interaction was examined. On the reaction of 50 micrometers drug and 500 micrometers nitrite at pH 3.0--3.4 and 37 degrees C for 4 h, the considerable formation of nitroso compounds was observed for ethambutol, cinnarizine and pyridinol carbamate. The reaction product of pyridinol carbamate and nitrite was remarkably mutagenic to Salmonella typhimurium TA100 in the absence of S-9 mix. Under conditions presumed to resemble those in the stomach after ingestion of a therapeutic dose of the drug, the formation of nitroso compounds was observed for ethambutol and significant mutagenicity was detected in the reaction product of pyridinol carbamate.

Benzothiazoles↗
PubMed1981

Formation of nitroso compounds and mutagens from tranquilizers by drug/nitrite interaction.

The formation of nitroso compounds and mutagens by drug/nitrite interaction was screened for 14 tranquilizers. The drug (0.05 M) was reacted with nitrite (0.5 M) at pH 3-3.5. After 4 h at 37 degrees C, nitroso compound formation was observed for flupentixol, chlordiazepoxide, spiperone, thiothixene, and chlorprothixene in more than 40% yield. Mutagenicity was found in the reaction products of opipramol, chlordiazepoxide, bromazepam, thiothixene, and carpipramine by the Ames assay using Salmonella typhimurium TA98 and TA100 as tester strains.

Drug Interactions↗
PubMed1980

Are nitrite and N-nitroso compounds in gastric juice risk factors for carcinoma in the operated stomach?

The concentration of nitrite and N-nitroso compounds was examined in the fasting gastric juice of 44 patients operated on for ulcer disease an average of 2.5 years previously and in 26 age-matched patients with healthy stomachs (controls). The concentration of nitrite and N-nitroso compounds in the gastric juice of the vagotomised patients did not differ from that of the controls. On the other hand, significant increases in nitrite concentrations were found in the gastric juice of patients managed by Billroth I or II procedures. The fraction of N-nitroso compounds was significantly increased only in the Billroth II resected stomach. These findings are relevant to the known cancer risk inherent in the gastric stump.

Bacteria↗
PubMedDate not supplied

Determination of N-nitroso compounds by high-performance liquid chromatography with postcolumn reaction and a thermal energy analyzer.

Carcinogenic nonvolatile N-nitroso compounds have been difficult to determine in foods and other consumer products because of the incompatibility of aqueous high-performance liquid chromatography (HPLC) mobile phases with the thermal energy analyzer (TEA), a sensitive and selective detector for N-nitroso compounds. A postcolumn technique has been developed that permits the use of aqueous mobile phases with an interfaced liquid chromatograph/TEA. This system was linear from 3.5 to 900 ng of N-nitrosoproline injected. Coefficients of variation of 3.0 and 5.1%, respectively, were obtained when N-nitrosoproline and N-nitrosotrimethylurea were repeatedly injected at the 80- to 90-ng level. Mixtures of volatile and nonvolatile N-nitroso compounds as well as N-nitrosodipeptides were separated and quantitated by HPLC/TEA with a water/acetonitrile gradient.

Chemistry Techniques, Analytical↗
PubMed1978

Non-volatile N-nitroso compounds in human feces.

A bacterial mutagen has been detected in ether extracts of freeze-dried feces of humans on Western diet. Several types of evidence suggest that nitroso compounds are present in human feces and the mutagen could be a nitroso compound. Ascorbic acid supplement in the diet reduces the levels of both the mutagens and nitroso compounds in the feces.

Ascorbic Acid↗
PubMed1988

The initiator tRNA acceptance assay as a short-term test for carcinogens. 3. Results with 69 N-nitroso compounds.

The activity of 69 carcinogenic and non-carcinogenic N-nitroso compounds was tested by the recently developed initiator tRNA acceptance assay for carcinogens. Of 51 carcinogens tested, 50 were active in the assay. Only N-nitrosopropylpropanolamine showed a false negativity. Eleven out of 14 tested non-carcinogenic compounds were not active in the assay, nitrosoethyl-tert-butylamine and nitrosoprolineethylester were positive. As calculated from these data, the sensitivity of the assay was 98.0%, specificity 84.6%, accuracy 95.4% and predictive value 94.4%. Comparison of relative carcinogenicities in animal bioassays with quantitative results (% stimulation of initiator tRNA charging) of the short-term test showed a good correlation for non-carcinogenic compounds and strong carcinogens. However, carcinogens of low and median potency could not be easily distinguished. A good correlation was obtained for three isomer N-nitrosomethylaminopyridines between the TD50-value and activity in the tRNA acceptance assay. The initiator tRNA acceptance assay thus seems preferable for recognizing and classifying carcinogenic and non-carcinogenic N-nitroso compounds than any other individual short-term test for carcinogenicity.

Animals↗
PubMed1989

[The problem of carcinogenic N-nitroso compounds--30 years old].

For 30 years a correlation between N-nitroso compounds and cancer in man has been suspected. Investigations of nitrate and nitrite in food and human gastric cancer were performed all over the world. Literature on nitrosamines and nitrosamides is abundant, but it is impossible to make a realistic assessment of the danger of N-nitroso compounds and their precursors for man. Restriction of unnecessary intake of nitrate through drinking water and food is in any case an important task of hygiene.

Animals↗
PubMed1997

N-nitroso compounds and man: sources of exposure, endogenous formation and occurrence in body fluids.

Based on recent analytical data, total human exogenous exposure to N-nitrosamines is estimated to be 1.10 mumol/day; the major exposure sources are the diet (0.79 mumol/may, 80-120 micrograms/day; 72%), occupational exposure (0.15-0.30 mumol/day; 25%), cigarette smoking (0.02 mumol/day, 3.4 micrograms/day; 2%), and miscellaneous minor sources, including pharmaceutical products, cosmetics, indoor and outdoor air (0.001 mumol/day, 0.1 micrograms/day; 1%). Excretion of apparent total N-nitroso compounds (ATNC) in healthy adults is estimated to be 1.30 +/- 1.05 mumol/day in urine and between 1.56 +/- 1.56 and 3.17 +/- 2.58 mumol/day in faeces. The excretion of volatile N-nitrosamines (N-nitrosodimethylamine), and N-nitrosamine acids and their derivatives (N-nitrososarcosine, N-nitrosoproline, N-nitrosothiazolidine-4-carboxylic acid and N-nitroso-2-methylthiazoline-4-carboxylic acid) accounts for approximately 0.03% and 16.0% of urinary ATNC, respectively. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanol and its O-glucuronide conjugate, two metabolites of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone present in urine of smokers, account for 0.2% of the urinary ATNC response; < 1.5 of the excretion of currently identified N-nitroso compounds in urine. The remaining N-nitroso compounds excreted in urine and those present in faeces are still unidentified. A crude mass balance between exogenous exposure and excretion in urine and faeces indicates that 45-75% of the total human exposure to N-nitroso compounds results through in vivo formation.

Environmental Exposure↗
PubMed1985

Studies in gastric carcinogenesis. III. The kinetics of nitrosation of gastric-juice components in vitro and their implications for the in vivo formation of N-nitroso compounds in normal and in hypochlorhydric populations.

Fasting human gastric juice was treated in vitro, at pH 2-7 and 37 degrees C for 2 h, with 5-100 microM sodium nitrite. Under these conditions (which simulated those occurring in vivo in normal or hypochlorhydric individuals), the formation of total N-nitroso compounds had the following characteristics: (i) it increased greatly at pH less than 3; (ii) it showed first-order dependence on nitrite concentration; (iii) it was faster at pH 7 than at pH 5. These observations are compatible with the N-nitroso compounds formed by the interaction of nitrite with gastric juice being N-nitrosamides or related compounds. Furthermore, based on the results of this study, it is suggested that in order for hypochlorhydria to give rise to increased formation of N-nitroso compounds in the stomach, it would be necessary for it to be accompanied by a greater than 5- to 10-fold increase in gastric nitrite concentration relative to that found in the normal population, a condition which is not necessarily fulfilled in all hypochlorhydric individuals or populations. The implications of this conclusion for the assessment of the role on gastric N-nitroso compounds in the etiology of gastric cancer are discussed.

Gastric Acid↗
PubMed1981

Quandtitative correlation among DNA damaging potency of six N-nitroso compounds and their potency in inducing tumor growth an bacterial mutations.

Six N-nitroso compounds (N-nitrosodimethylamine, N-nitrosodiethylamine, N-nitrosodi-n-propylamine, N-nitroso-N-methylurea, N-nitrosopyrrolidine, and N-nitrosodi-n-butylamine) were tested in rats for liver DNA damaging activity by the alkaline elution technique. On molar basis their DNA damaging potency was found to decrease in the above order, and to vary over a 28-fold range. The elaboration of homogenous data available from literature showed that the carcinogenic potency of the 6 N-nitroso compounds varied over an 18-fold range, and that their mutagenic potency varied over a 490-fold range. Regression analysis indicated that correlation between carcinogenic and DNA damaging potencies was positive but at a low significance level, while the correlation between carcinogenic and mutagenic potencies was negative.

Animals↗
PubMedDate not supplied

Precautions to be taken in the analysis of total N-nitroso compounds.

Methodologies used to assess N-nitroso compounds as a group by chemical denitrosation with hydrogen bromide in glacial acetic acid have been described. Carrying out these analyses without precautions can cause considerable variations in results. Some pitfalls must be avoided in order to obtain valuable results and accurate interpretations.

Chemical Fractionation↗
PubMed1996

Nitrite, N-nitroso compounds, and other analytes in physiological fluids in relation to precancerous gastric lesions.

Levels of gastric juice nitrite, several urinary N-nitroso compounds, and other analytes were examined among nearly 600 residents in an area of Shandong, China, where precancerous gastric lesions are common and rates of stomach cancer are among the world's highest. Gastric juice nitrite levels were considerably higher among those with gastric juice pH values above 2.4 versus below 2.4. Nitrite was detected more often and at higher levels among persons with later stage gastric lesions, especially when gastric pH was high. Of those with intestinal metaplasia, 17.5% had detectable levels of gastric nitrite, while this analyte was detected in only 7.2% of those with less advanced lesions. Relative to those with undetectable nitrite, the odds of intestinal metaplasia increased from 1.5 (95% confidence interval = 0.6-4.1) to 4.1 (95% confidence interval = 1.8-9.3) among those with low and high nitrite concentrations, respectively. Urinary acetaldehyde and formaldehyde levels also tended to be higher among those with more advanced pathology, particularly dysplasia. However, urinary excretion levels of total N-nitroso compounds and several nitrosamino acids differed little among those with chronic atrophic gastritis and intestinal metaplasia and dysplasia, consistent with findings from recent studies in the United Kingdom, France, and Colombia. The data from this high-risk population suggest that elevated levels of gastric nitrite, especially in a high pH environment, are associated with advanced precancerous gastric lesions, although specific N-nitroso compounds were not implicated.

Adult↗
PubMed1994

Nitrate, nitrite and N-nitroso compounds.

A risk assessment has been made on nitrate, nitrite and N-nitroso compounds encountered in the human diet. Vegetables constitute a major source of nitrate providing over 85% of the average daily human dietary intake. Nitrite and N-nitroso compounds present in the diet contribute relatively small amounts to the body burden and the major source of these biologically reactive compounds is derived from the bacterial and mammalian metabolism of ingested nitrate. Additionally, endogenous synthesis provides an important source contributing to the body burden of nitrate. Data from animal toxicological studies, human effects and epidemiological surveys have been reviewed and evaluated. It is concluded that there is no firm scientific evidence at present to recommend drastic reductions beyond the average levels of nitrate encountered in vegetables grown in keeping with good agricultural practice. Recommendations have also been made for further animal and human studies to be carried out to elucidate the potential risks to man from ingested nitrate.

Animals↗
PubMed1997

DNA single strand breaks by aromatic nitroso compounds in the presence of thiols.

Aromatic nitroso compounds, nitrosobenzene (NB), N,N-dimethyl-4-nitrosoaniline (DMNA) and 3,5-dibromo-4-nitrosobenzene sulfonate (DBNBS), caused DNA single strand breaks in the presence of thiol compounds. The strand breaking was inhibited completely by free radical scavenger ethanol. Electron spin resonance (ESR) studies showed that hydronitroxyl (or sulfur-substituted nitroxyl) radicals were generated in the early stage of the interactions. Formation of these radicals was not inhibited by ethanol, indicating that these radicals did not directly contribute to the strand breaking. The DNA strand breaking was inhibited partially by superoxide dismutase and catalase under the limited conditions, but not by removal of oxygen from or addition of metal chelators to the reaction mixture. By ESR-spin trapping technique using 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), the DMPO-OH spin adduct was detected. Formation of the spin adduct was inhibited by superoxide dismutase and catalase. The hydronitroxyl (or the sulfur-substituted nitroxyl) radicals may reduce oxygen into active oxygen species and also transformed by themselves into other unidentified free radical species to cause the DNA strand breaks.

Animals↗