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PubMed2002

Intake of volatile N-nitrosamines and their ability to exogenously synthesize in the diet of inhabitants from high-risk area of esophageal cancer in southern China.

OBJECTIVE: Nan'ao County in Guandong Province is a high-risk area of esophageal cancer in Southern China. Of the suspected etiological factors in the environment, N-nitrosamines and their precursors have received the greatest attention. METHODS: Sixty samples of the diet ingested by the inhabitants were collected and detected for volatile N-nitrosamines and their precursors. Five N-nitrosamines detected by Gas Chromatography-Thermal Energy Analyzer were N-nitrosodimethylamine, N-nitrosodiethylamine, N-nitrosopyrrolidine, N-nitrosopiperidine and N-nitrosomethyl-benzylamine. RESULTS: The average content of 5 volatile N-nitrosamines in the diet was 312.0 micrograms/kg (median). The daily intake of the nitrosamines was 286.5 micrograms/head/day. Only the ability to exogenously synthesize N-nitrosopiperidine was powerful among 5 volatile N-nitrosamines. By a computerized stepwise regression analysis and curve fitting, we studied the correlation among the nitrosamines, the precursors and the major food items in the samples. CONCLUSION: It demonstrated that a relatively high content of volatile N-nitrosamines was present in the diet collected in the area.

Adult↗
PubMed1978

Rapid formation of N-nitrosamines from nitrogen oxides under neutral and alkaline conditions.

The formation of carcinogenic N-nitrosamines in neutral and alkaline aqueous solutions (pH 6-14) at 25 degrees C is reported using dissolved N2O3 and N2O4 gases. These reactions are very much faster than those with acidified nitrite: typically, 2 X 10(-3) M amine gives ca. 10-50% N-nitrosamine in a few seconds with 5-20 fold excess of nitrogen oxide. The N-nitrosamine yield in 0.1 M sodium hydroxide is independent of amine basicity from pKA 11.2-0.99, but decreases with decreasing pH of the reaction solution for the more basic amines. Significantly, N-nitrosamine yields are not lowered with diluted nitrogen oxides (1000 ppm) and moderately basic amines (eg. N-methylpiperazine) react readily at physiological pH. The mechanism by which these reactions occur is discussed, with particular reference to the existence of two reactive tautomeric forms of N2O3 and N2O4. The formation of carcinogenic N-nitrosamines from NO in ethanol at 25 degrees C is also reported. These reactions are slow in the absence of air (oxygen), I2 or metal salts. Oxygen accelerates nitrosation by converting NO via NO2 to either N2O3 or N2O4, but both I2 and metal salts are effective under anaerobic conditions, where reaction rates are virtually independent of amine basicity but depend on the nature of the added reagent. The most effective substance is I2, which gives quantitative yields of N-nitrosamine in a few minutes at 25 degrees C by forming the reactive nitrosyl iodide (NOI) reagent. Acceleration in ethanol at 25 degrees C is also observed with AgI, CuI, CuII, ZnII, FeIII and CoII salts, among others, with substantial amounts of N-nitrosamine being produced in ca. 30-300 min. Metal iodides intervene by way of the NOI reagent, as for I2, but other salts require a mechanism involving reaction between a metal-amine complex and NO, itself. The results show that carcinogenic N-nitrosamines may form under a much wider range of experimental conditions than suspected hitherto. Their relevance to human exposure is discussed, with particular reference to urban pollution and the effect of dietary antioxidants.

Amines↗
PubMed1982

Nitrosamines and rubber.

Occupational exposure to N-nitrosamines in the rubber industry was first reported by Fajen et al. (1979). In order to study the origin and formation of nitrosamines in this industry, chemicals and industrial products, as well as the air in various working areas, were analysed (Spiegelhalder et al., 1980). All chemicals used for rubber compounding contain nitrosamines if they are derivatives of secondary amines; e.g., tetramethylthiurame, zinc-diethyldithiocarbamate or N-oxydiethylene benzothiazolylsulfenamide. All rubber products containing these dialkyl amine derivatives exhibited considerable levels of the corresponding nitrosamines. Accordingly, variable concentrations of airborne nitrosamines could be detected at places where rubber products are manufactured or stored. The nitrosamines found correspond to the compounded chemicals. The original nitrosamine level in rubber chemicals is not high enough to explain the amounts found in rubber products and in air, so that additional nitrosation must occur. The responsible nitrosating agents are described. Preliminary results show that, in most cases, the elimination of nitrosating agents or the use of different rubber chemicals can drastically reduce nitrosamine levels in rubber products and in working areas.

Air Pollutants↗
PubMed1981

Metabolic fate of N-butyl-N-(4-hydroxybutyl)nitrosamine homologs in the rat, in relation to their organotropic carcinogenicity to the urinary bladder.

The metabolic fate of alkyl homologs (alkyl=methyl, ethyl, propyl, pentyl, and tert-butyl) of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), a potent bladder carcinogen, was investigated in the rat, in order to elucidate any possible correlation of structure and metabolism with organospecific carcinogenicity to the urinary bladder of these N-nitrosamines. They were extensively metabolized in the rat, no unchanged compounds being found in the urine. The metabolic pattern of these alkyl homologs of BBN was essentially similar to that of BBN. Their principal urinary metabolite was the corresponding N-alkyl-N-(3-carboxypropyl)nitrosamine except in the case of the pentyl homolog. Minor metabolites characterized were subsequent transformation products of the principal metabolite by beta-oxidation according to the Knoop mechanism (i.e., N-alkyl-N-(2-hydroxy-3-carboxypropyl)nitrosamine, N-alkyl-N-(carboxymethyl)nitrosamine and N-alkyl-N-(2-oxopropyl)nitrosamine) and the glucuronic acid conjugate excretion of the N-alkyl-N-(c-carboxypropyl)nitrosamine with selective induction of bladder cancer by the N-alkyl-N-(4-hydroxybutyl)nitrosamine in rats is discussed.

Animals↗
PubMed1987

Urinary carcinogen [nitrosamine] production in a rat animal model for ureterosigmoidostomy.

Tumor development at the site of ureterointestinal anastomosis is a recognized complication in patients undergoing ureterosigmoidostomy. In order to explore the hypothesis that carcinogens (nitrosamines) may be a factor in ureterosigmoidostomy, female Sprague-Dawley rats (n = 125) underwent urethral ligation, bladder dome resection and anastomosis of the bladder trigone to an opening in the anterior rectosigmoid wall. Biweekly nitrosamine determinations were performed on the resultant urine-feces slurry by gas chromatography up to thirty-two weeks post surgery. Nitrosamine (N,N-dimethylnitrosamine) was noted as early as two weeks after surgery in 39% (11/28) of rats. One hundred percent of animals consistently demonstrated nitrosamine by week 14 (32 rats). Nitrosamine levels increased throughout the study with a peak level after thirty-two weeks of 0.275 micrograms./ml. Only a portion (n = 40) of the total animal population was deemed suitable for pathologic examination secondary to animal demise and autolysis at autopsy related to infection and obstruction. In these animals, no adenocarcinoma was found although hyperplastic changes and metaplastic changes were demonstrable at nine days and eight weeks respectively. In one animal a grade I transitional cell papilloma was identified after eight weeks. Control animals demonstrated no nitrosamine production. In vitro combinations of rat urine and feces yielded nitrosamine after six weeks. The absence of adenocarcinoma tumor development is believed indirectly related to animal demise in that not enough time had elapsed to allow significant tumor development. This study lends support to the concept that nitrosamines may play a role in the development of hyperplasia, dysplasia and eventual neoplasia in ureterosigmoidostomy.

Adenocarcinoma↗
PubMed2000

Dietary exposure to nitrite and nitrosamines and risk of nasopharyngeal carcinoma in Taiwan.

Previous studies of nasopharyngeal carcinoma (NPC) have found elevated risks with higher consumption of salted fish and preserved foods, particularly during childhood. These foods can contain high levels of nitrosamines; however, most studies have not estimated exposure to nitrosamines directly. We conducted a case-control study in Taiwan to evaluate dietary intakes and NPC risk. A total of 375 cases (99% response rate) and 327 controls (88% response rate) were interviewed about their diet as an adult and at age 10 using a food-frequency questionnaire. We interviewed mothers of participants about their child's diet at age 10, age 3 and during weaning and the mother's diet while she was breast-feeding. Mothers of 96 cases and 120 controls were interviewed. Nitrosamine and nitrite levels were assigned to 66 foods based on published values. Intake of nitrosamines and nitrite as an adult was not associated with risk of NPC. High intakes of nitrosamines and nitrite during childhood and weaning were associated with increased risks of NPC for foods other than soy products. Adjusted odds ratios for the highest quartile were 2.2 [95% confidence interval (CI) 0.8-5.6] for age 10, 2.6 (95% CI 1.0-7.0) for age 3 and 3.9 (95% CI 1.4-10.4) for weaning diet. Intakes of nitrite and nitrosamines from soybean products during childhood and weaning were inversely associated with risk. Soybeans contain known inhibitors of nitrosation, and thus may explain the inverse association we observed. Our results suggest that nitrosamine and nitrite intake during childhood may play a role in the development of NPC.

Adult↗
PubMed2005

Tobacco-specific nitrosamines in smokeless tobacco products marketed in India.

Smokeless tobacco products are a known cause of oral cancer in India. Carcinogenic tobacco-specific nitrosamines in these products are believed to be at least partially responsible for cancer induction, but there have been no recent analyses of their amounts. We quantified levels of 4 tobacco-specific nitrosamines, N'-nitrosonornicotine (NNN), N'-nitrosoanatabine (NAT), N'-nitrosoanabasine (NAB) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), in 32 products marketed currently in India. Levels of nitrate, nitrite and nicotine were also determined. The highest levels of tobacco-specific nitrosamines were found in certain brands of khaini, zarda and other smokeless tobacco products. Concentrations of NNN and NNK in these products ranged from 1.74-76.9 and 0.08-28.4 microg/g, respectively. Levels of tobacco-specific nitrosamines in gutka were generally somewhat lower than in these products, but still considerably higher than nitrosamine levels in food. Tobacco-specific nitrosamines were rarely detected in supari, which does not contain tobacco, or in tooth powders. The results of our study demonstrate that exposure to substantial amounts of carcinogenic tobacco-specific nitrosamines through use of smokeless tobacco products remains a major problem in India.

Carcinogens↗
PubMed1986

N-nitrosamines and residual nitrite in cured meats from the Dutch market.

A total of 140 samples of 16 kinds of cured meats were analyzed for contents of residual nitrite and N-nitrosamines. Nitrite was determined by reaction with sulfanilamide/naphthylethylenediamine and colorimetric measurement. N-nitrosamines were isolated from the samples by vacuum distillation and determined by gas-chromatography with chemiluminescence detection (GC-TEA). In six samples no nitrite was detectable (less than 1 mg NaNO2/kg), the remaining samples contained 1-140 mg NaNO2/kg, median value 6.8 mg/kg. In 46 samples (33%) no N-nitrosamines were detected, i.e. less than 0.1-0.5 microgram/kg of the individual nitrosamines, depending upon their structure. N-nitrosodimethylamine (NDMA) was the nitrosamine present most frequently, in 75 samples, contents were 0.1-0.9 microgram/kg, mean 0.3 microgram/kg. Other N-nitrosamines found were: N-nitrosopiperidine (NPIP), 10 times, 0.3-25 micrograms/kg; N-nitrosodiethylamine (NDEA), three times, 0.2-0.9 microgram/kg; N-nitrosopyrrolidine (NPYR), three times, 1.3-4.2 micrograms/kg; N-nitrosomorpholine, once, 0.7 microgram/kg and N-nitrosothiazolidine (NTHZ), 36 times, 0.5-91 micrograms/kg, mean 5.7 micrograms/kg. NTHZ was found most often and with the highest contents in smoked products. Frying of bacon and cured, smoked pork bellies led to substantially increased levels of NPYR in both products, and for the pork bellies also of NTHZ. In five samples of cured, smoked pork bellies after frying NTHZ-contents of 3.6-490 micrograms/kg (mean 179) were found. No correlation between residual nitrite levels and N-nitrosamine contents could be established. Investigations during the nineteen seventies gave much higher levels for NDMA, NDEA, NPIP and NPYR in Dutch cured meats than now found; at that time NTHZ was not measured.

Animals↗
PubMed1976

[Quantitative determination of volatile nitrosamines in cigarette smoke (author's transl)].

Volatile nitrosamines from the smoke of different cigarettes were enriched by manifold clean-up procedures. Amines obtained after acid catalyzed denitrosation were transformed to fluorescent derivates of 7-chloro-4-nitrobenzofuranzane (NBD-Cl). These NBD-amines separated on polyamid sheets were fluorimetrically determined with a chromatogram-spectrophotometer. Recovery rates of 60--80% were found for the different nitrosamines in cigarette smoke condensate. The following nitrosamines were quantitatively determined: N-nitrosodimethylamine, N-nitrosodiethylamine, N-nitrosopiperidine, N-nitrosopyrrolidine, N-nitrosoethylmethylamine, N-nitroso-ethyln-propylamine and N-nitroso-methyl-n-propylamine, N-nitroso-ethyl-n-propylamine and N-nitroso-methyl-n-propylamine. The last mentioned nitrosamine was proved for the first time in cigarette smoke. At the same time correlations between the nitrosamine content of the corresponding tobacco or condensate and the content of nitrate, total nitrogen, nicotine, volatile bases and ammonia were investigated. The nitrate content as well as the content of volatile bases showed an influence on the nitrosamine yield. The content of the different nitrosamines varied cosiderably depending on tobacco origin, so that a NNO-determination is recommended as index.

Methods↗
PubMed1996

Selective determination of volatile N-nitrosamines by derivatization with diethyl chlorothiophosphate and gas chromatography with flame photometric detection.

A selective and sensitive method was developed for the determination of volatile N-nitrosamines by gas chromatography (GC). After denitrosation of N-nitrosamines with hydrobromic acid, the resulting secondary amines were converted into their N-diethylthiophosphoryl derivatives and then measured by GC using a DB-1701 capillary column with flame photometric detection. The calibration graphs for N-nitrosamines in the range 0.05-1 nmol were linear and sufficiently reproducible for quantitative determination. This method was successfully applied to cigarette smoke samples without prior clean-up. N-Nitrosamines and secondary amines were completely separated by extraction with diethyl ether containing 25% 2-propanol. Overall recoveries of N-nitrosamines added to cigarette smoke samples were 83-110%. By using this method, N-nitrosamines in these samples could be determined without any interference from coexisting substances. Analytical results for the contents of N-nitrosamines and secondary amines in mainstream and sidestream smokes of several cigarettes are presented.

Amines↗
PubMed1996

Inhibition of mutagenicity of N-nitrosamines by tobacco smoke and its constituents.

Tobacco smoke is a complex chemical mixture including pyridine alkaloids and N-nitrosamines, with the concentration of the former several orders of magnitude higher that that of the N-nitrosamines. The major biologically important N-nitrosamines present in tobacco smoke are N-nitrosodimethylamine (NDMA), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N(1)-nitrosonornicotine (NNN). These nitrosamines require metabolic activations by cytochrome P-450s for the expression of mutagenicity. Although nicotine, the major pyridine alkaloid in tobacco, has been shown to inhibit the metabolic activation of NNK, its effect on the mutagenicity of NNK and other N-nitrosamines has not been reported, In the present study, the ability of three pyridine alkaloids (nicotine, cotinine, nornicotine) and aqueous cigarette smoke condensate extract (ACE) to inhibit the mutagenicity of tobacco-related N-nitrosamines was tested on Salmonella typhimurium strain TA1535 in the presence of a metabolic activation system (S9). All three of the pyridine alkaloids tested, as well as ACE, inhibited the mutagenicity of NDMA and NNK, but not NNN, in a concentration-dependent manner. The induction of SCEs in mammalian cells (CHO) by NNK in the presence of metabolic activation was also significantly reduced by nicotine and cotinine. None of the observed reductions in mutagenicity could be explained by cytotoxicity. These results demonstrate that tobacco smoke contains chemicals, pyridine alkaloids and other unidentified constituent(s), which inhibit the mutagenicity of N-nitrosamines.

Animals↗
PubMed1997

Nasal cavity carcinogenesis by N-nitrosamines: a critical appraisal.

This review is a critical appraisal of our current knowledge on nasal cavity carcinogenesis by nitrosamines. The pathology and pathogenesis of nitrosamine-induced tumors in the nasal cavity of rodents is summarized while controversies on the underlying molecular mechanisms are discussed in more detail. Investigations on the distribution of metabolically competent cell types, the cellular site(s) of nitrosamine metabolism, as well as reports on the cellular distribution and persistence of DNA-adducts strongly suggest that DNA-adducts formed from reactive metabolites are not immediately responsible for the genesis of nasal cavity tumors. A preexisting high proliferative ability has also been suggested as a factor rendering certain cell types more susceptible to the carcinogenic actions of nitrosamines in the nasal cavity. However, this hypothesis has been clearly rejected by more recent investigations. Recent studies have shown that nitrosamines can stimulate the secretion of growth factors via interaction with neurotransmitter receptors in the lungs and that this molecular mechanism is an important factor in determining the histological phenotype of the developing lung tumors. In light of the fact that secretory cells are the main sites of DNA-adduct accumulation and toxic lesions in the nasal cavities of nitrosamine treated rodents, it is suggested that similar mechanisms may mediate the genesis of nitrosamine-induced nasal cavity tumors.

Animals↗
PubMed1981

Photosuicide inactivation of acetylcholinesterase by nitrosamine derivatives.

Methyl(acetoxymethyl)nitrosamine and methyl-(butyroxymethyl)nitrosamine are respectively substrate (KM - 10(-2) M) and competitive inhibitor (Ki = 2 x 10(-3) M) of electric eel acetylcholinesterase (EC 3.1.1.7). Irradiation of an incubation mixture of this enzyme with either nitrosamine leads to an irreversible loss of enzyme activity. The inactivation rates are dependent on photolysis wavelength, light intensity, and inhibitor concentration. Experiments where acetylcholinesterase was radioactively labeled by [14C]-methyl(acetoxymethyl)nitrosamine show that the incorporation of 1 mol of radioactive label per active site is sufficient to cause complete enzyme inactivation irrespective of the reaction conditions used. Methyl(acetoxymethyl)nitrosamine shows no affinity for horse serum butyrylcholinesterase (EC 3.1.1.8) while methyl(butyroxymethyl)nitrosamine is a competitive inhibitor (Ki = 2 x 10(-3) M), but no irreversible inhibition is induced by the action of light. We propose that a suicide type of inhibition [Bloch, K. (1969) Acc. Chem. Res. 2, 193-198] is responsible for the inactivation of acetylcholinesterase, based on photoactivation of nitrosamines only when associated with an acidic hydrogen of the active site.

Animals↗
PubMedDate not supplied

N-nitrosamines in snuff and chewing tobacco on the Swedish market in 1983.

Snuff and chewing tobacco on the Swedish market in 1983 were analysed for tobacco-specific and volatile N-nitrosamines using gas chromatography--thermal energy analysis. All 36 samples of snuff analysed were found to contain detectable levels of N'-nitrosonornicotine, N'-nitrosoanatabine, N'-nitrosoanabasine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. Total tobacco-specific N-nitrosamine levels between 2.5 and 51 mg/kg wet weight were found, the mean level being 8.8 mg/kg. Detectable levels of at least two of the four tobacco-specific N-nitrosamines were found in all 18 samples of chewing tobacco analysed. The total concentration of tobacco-specific N-nitrosamines found in chewing tobacco was between 0.1 and 7.8 mg/kg, the mean level being 2.1 mg/kg. The levels of volatile N-nitrosamines found in the 54 samples of snuff and chewing tobacco were very much lower--most of the samples contained less than 10 micrograms/kg and the highest concentration found was 550 micrograms/kg. Since snuff and chewing tobacco contain relatively high levels of carcinogenic N-nitrosamines and there is evidence of an association between the use of these tobacco products and human cancer, snuff and chewing tobacco users should be warned about the possible cancer risk involved in their habit. In addition, efforts should be made to reduce the levels of N-nitrosamines in snuff and chewing tobacco and the formation of these substances in the body from precursors originating from these tobacco products.

Chromatography, Gas↗
PubMed1986

Carcinogenicity of N-alkyl-N-(1-hydroperoxyalkyl) nitrosamines after intravenous injections in F344 rats.

As model compounds of alpha-hydroxy N-nitrosamines, four alpha-hydroperoxy N-nitrosamines were tested for their carcinogenic potential in F344 rats by i.v. injections. Correlation between chemical structure and carcinogenic potencies with respect to target organs was examined. Compounds used in this study were N-methyl-N-(hydroperoxymethyl)nitrosamine (MHPMN), N-ethyl-N-(1-hydroperoxyethyl)nitrosamine (EHPEN), N-propyl-N-(1-hydroperoxypropyl)nitrosamine (PHPPN) and N-butyl-N-(1-hydroperoxybutyl)nitrosamine (BHPBN). All chemicals were dissolved in distilled water and rats received 10 X 1 weekly i.v. injections of these chemicals (10 X 1 weekly injection of 5 mg/kg of MHPMN or equimolar amounts of other chemicals). Lung tumors were detected in all groups of both sexes and the incidences were 100% in each group. Thyroid tumors were also observed with relatively high incidences in treated groups except BHPBN. In the control group, tumors were observed mainly in the testis or uterus, and only two lung tumors and one thyroid tumor were observed in females. Histologically, all lung tumors in the MHPMN group were adenocarcinomas, squamous cell carcinomas or a mixture of both types. In the EHPEN, PHPPN and BHPBN groups, especially in females, incidences of carcinomas decreased as the length of the alkyl chain of the compounds, and most of lung tumors in females of the PHPPN and BHPBN groups were adenomas. Many of the thyroid tumors observed in the treated groups were follicular adenomas/carcinomas, whereas C-cell adenomas were the most common type of spontaneous thyroid tumors in this strain of rats. These target organs were similar to those of alpha-acetoxy N-nitrosamines reported previously. The results indicate that the carcinogenic activities of these chemicals depend on the length of the alkyl chain and that organ specificity of these chemicals may differ from those of their mother compounds.

Animals↗
PubMed1988

Tobacco-specific nitrosamines, an important group of carcinogens in tobacco and tobacco smoke.

Tobacco-specific nitrosamines are a group of carcinogens that are present in tobacco and tobacco smoke. They are formed from nicotine and related tobacco alkaloids. Two of the nicotine-derived nitrosamines, NNK and NNN, are strong carcinogens in laboratory animals. They can induce tumors both locally and systemically. The induction of oral cavity tumors by a mixture of NNK and NNN, and the organospecificity of NNK for the lung are particularly noteworthy. The amounts of NNK and NNN in tobacco and tobacco smoke are high enough that their total estimated doses to long-term snuff-dippers or smokers are similar in magnitude to the total doses required to produce cancer in laboratory animals. These exposures thus represent an unacceptable risk to tobacco consumers, and possibly to non-smokers exposed for years to environmental tobacco smoke. The permission of such high levels of carcinogens in consumer products used by millions of people represents a major legislative failure. Indeed, the levels of tobacco-specific nitrosamines in tobacco are thousands of times higher than the amounts of other nitrosamines in consumer products that are regulated by government authorities. Although the role of tobacco-specific nitrosamines as causative factors in tobacco-related human cancers cannot be assessed with certainty because of the complexity of tobacco and tobacco smoke, several lines of evidence strongly indicate that they have a major role, especially in the causation of oral cancer in snuff-dippers. Epidemiologic studies have demonstrated that snuff-dipping causes oral cancer. NNK and NNN are quantitatively the most prevalent known carcinogens in snuff, and they induce oral tumors when applied to the rat oral cavity. A role for NNK in the induction of lung cancer by tobacco smoke is likely because of its organospecificity for the lung. Tobacco-specific nitrosamines may also be involved in the etiology of tobacco-related cancers of the esophagus, nasal cavity, and pancreas. Because they are derived from nicotine, and therefore should be associated only with tobacco, tobacco smoke and other nicotine-containing products, tobacco-specific nitrosamines as well as their metabolites and macromolecular adducts should be ideal markers for assessing human exposure to, and metabolic activation of, tobacco smoke carcinogens. Ongoing research has demonstrated the formation of globin and DNA adducts of NNK and NNN in experimental animals. Sensitive methods for the detection and quantitation of these adducts in humans would provide an approach to assessing individual risk for tobacco-related cancers.(ABSTRACT TRUNCATED AT 400 WORDS)

Humans↗
PubMed1992

[Exposure level of N-nitrosamines in the gastric juice and its inhibition by vitamin C in high risk areas of esophageal cancer].

A total of 391 gastric juice samples was collected from Ji Yuan and An Shi counties, high and medium risk areas of esophageal carcinoma in Henan province. NDMA, NDEA, NMBzA, NPip and unknown compounds were assayed in the fasting gastric juice. Among these nitrosamines, NMBzA, NPyr and NPip were specific in inducing esophageal cancer in animals. The amount of nitrosamines in the gastric juice collected from Ji Yuan county was higher than that from An Shi county. The exposure level of nitrosamines of subjects from these two localities were significantly different (P < 0.001). There was a positive relationship between the nitrosamines exposure level and esophageal cancer mortality rate. The amount of gastric N-nitrosamines from An Shi subjects as treated with vitamin C was reduced. It is evident that vitamin C can inhibit N-nitrosamine formation in the stomach, thereby, reducing the N-nitrosamines exposure level.

Adult↗
PubMed1992

Molecular effects of nitrosamine toxicity.

Nitrosamines are toxic chemical compounds found low in quantity, but widespread in the environment. This work investigated the kinetics of chemical reaction of activated nitrosamines with various organic substrates. The mechanism by which nitrosamines react demonstrates possible pathways in which the toxicity is expressed. Once activated nitrosamines are very reactive. Chemical compounds which can act as nucleophilic substrates may be alkylated by the activated nitrosamines. A broad category of chemical compounds are shown to be suitable substrates for nitrosamine induced alkylation. This large category of substrates suggests a substantial potential for toxic activity in vivo. By investigating the reaction kinetics of activated nitrosamines a greater understanding of their toxic effects may be possible.

Alkylating Agents↗