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At least 523 records · Page 29Linked to original sources
PubMed1992

[Fungi N-nitrosamines and mutagens in the extract of the sour corn-soybean cakes from high incidence area of stomach cancer].

Sour corn-soybean cake is the main food of the inhabitants in high incidence area of stomach cancer in Linqu county Shandong province. In the extract of the sour corn-soybean cakes, twelve mycotoxin-producing fungi and 3 N-nitrosamines (NDMA, NDEA, NMEA) were detected and the finding rates of the fungi and the N-nitrosamines were 93.3% and 92.3%, respectively; the concentration of NDMA was 0.4-3.8 ng/ml, NDEA 0.2-8.1 ng/ml, and NMEA 0.3-1.4 ng/ml. The positivity rate of the Ames test (most positive materials were direct mutagens) was 44.12%. The experimental results showed that the extract of the sour corn-soybean cakes containing carcinogenic and mutagenic subjects could have some causal relationship with the incidence of stomach cancer.

Food Microbiology↗
PubMed1991

[Non-volatile nitrosamines in some foods from Linxian County].

For the incidence of non-volatile nitrosamines in the staple foods and vegetables, corn, millet, turnip and turnip chips collected from Linxian County Henan Province, a high incidence area of esophageal cancer, were collected, analyzed and compared with the foods from Huairou County Beijing, a low risk area. Nitrososarcosine (NSAR), nitrosoproline (NPRO) and two unknown non-volatile compounds were found in the food samples from Linxian, and the levels of NSAR in corn ranged 0.7-1.1 ppb and in turnip chips ranged 20.5-962.5 ppb. NSAR level detected in corn samples from Huairou County was not significantly different from that of Linxian. The possibility that the high content of nitrosamines in turnip chips is due to microbial infections is discussed.

Nitrosamines↗
PubMed1991

Quantification of 4-hydroxy-1-(3-pyridyl)-1-butanone released from human haemoglobin as a dosimeter for exposure to tobacco-specific nitrosamines.

A method was developed to quantify globin adducts of the tobacco-specific nitrosamines 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN). Globin adducts of NNK and NNN release 4-hydroxy-1-(3-pyridyl)-1-butanone (HPB) after mild treatment with a base. HPB was analysed as its pentafluorobenzoate by capillary column gas chromatography with detection by negative-ion chemical ionization-mass spectrometry and selected-ion monitoring. The detection limit for HPB-pentafluorobenzoate was approximately 1 fmol/injection. The method was applied to haemoglobin from snuff dippers, smokers and nonsmokers. Adduct levels were highest in snuff dippers (517 +/- 538 fmol HPB per gram haemoglobin), followed by smokers (79 +/- 189 fmol HPB per gram haemoglobin) and nonsmokers (29.3 +/- 25.9 fmol HPB per gram haemoglobin). The method will be useful in assessing the role of tobacco-specific nitrosamines as causes of cancer in smokers and snuff dippers.

Environmental Monitoring↗
PubMed1991

Dietary sources of N-nitrosamines in a high-risk area for oesophageal cancer--Kashmir, India.

Samples of foods consumed frequently in Kashmir, a high-risk area for oesophageal cancer, were analysed for the presence of volatile N-nitrosamines. Relatively high levels of N-nitrosodimethylamine (NDMA), N-nitrosopiperidine (NPIP) and N-nitrosopyrrolidine (NPYR) were detected in smoked fish (20 micrograms/kg NDMA), sun-dried spinach (5.8 micrograms/kg NDMA; 23.8 micrograms/kg NPIP), sun-dried pumpkin (24.6 micrograms/kg NPYR) and dried, mixed vegetables (10 micrograms/kg NDMA). The possible role of N-nitrosamines in the etiology of oesophageal cancer in Kashmir is discussed.

Diet↗
PubMed1991

Analysis of volatile N-nitrosamines in beer and food in China.

Capillary gas chromatography-thermal energy analysis was used for the study of volatile N-nitrosamines in comestibles. The finding of a comparatively high content of N-nitrosodimethylamine in some Chinese beers confirms the results of other authors. We describe studies of Chinese foods and environmental samples carried out in this laboratory in collaboration with epidemiological groups. The concentrations of N-nitrosamines could be correlated with mortality from digestive cancer.

Beer↗
PubMed1991

Enzyme mechanisms in the metabolism of nitrosamines.

Many nitrosamines are metabolized by cytochromes P450, one of which (P450IIE1) has received much attention because of its role in the metabolic activation of N-nitrosodimethylamine. This enzyme exists in man, rat, mouse, hamster and other animal species. It is inducible by fasting, diabetes and exposure to ethanol, acetone, isoniazid, benzene and other chemicals. P450IIE1 is responsible for the low Km form of N-nitrosodimethylamine demethylase and is the major enzyme catalysing the metabolic activation of this carcinogen. In addition, P450IIE1 is the most active P450 species known in the metabolism of N-nitrosoethylmethylamine and N-nitrosopyrrolidine. In the metabolism of N-nitrosobutylmethylamine, P450IIE1 preferentially oxidizes the methyl group over the butyl group, whereas P450IIB1 efficiently oxidizes both the methyl and butyl groups. P450IIB1 also catalyses the alpha-oxygenation of both the pentyl and methyl groups of N-nitrosopentylmethylamine, forming pentaldehyde and formaldehyde at a rate ratio of 2:1, as well as oxygenation at other carbons of the pentyl group. Many nitrosamines are effectively activated in nonhepatic target tissues. The metabolism of 4-(N-nitroso-methylamino)-1-(3-pyridyl)-1-butanone in lung and nasal microsomes is discussed.

Animals↗
PubMed1991

Metabolic denitrosation of N-nitrosamines: mechanism and biological consequences.

NADPH-dependent microsomal metabolism of N-nitrosamines results in both oxidative dealkylation and denitrosation of the molecule. For denitrosation, two enzymatic mechanisms have been proposed: (i) cytochrome P450 (P450)-dependent one-electron reduction of the nitrosamine molecule, resulting in the formation of nitric oxide (NO) and secondary and primary amine, and (ii) liberation of NO via an oxidative mechanism mediated by a P450-dependent one-electron abstraction. In order to clarify the mechanism of denitrosation, the metabolism and kinetics of N-nitrosodibenzylamine (NDBzA) and its corresponding secondary amine dibenzylamine were studied. The main metabolites of NDBzA are benzaldehyde, the primary amine benzylamine and nitrite. An important finding is that benzaldehyde is generated more rapidly from dibenzylamine than from the parent NDBzA. During reductive denitrosation of NDBzA, the oxygen atom in benzaldehyde is derived from air, while benzaldehyde generated via the oxidative mechanism of denitrosation receives its oxygen atom from water due to hydrolysis of the intermediary benzylidenebenzylamine. Microsomal incubation of NDBzA in buffer containing 18O-H2O resulted in no incorporation of 18O from water into benzaldehyde, which could be related to the formation of the corresponding benzaldehyde, which could be related to the formation of the corresponding benzylidenebenzylamine. It is concluded that NDBzA is denitrosated by the proposed reductive mechanism. Current belief is that denitrosation leads to detoxification of the NA molecule; however, toxic effects cannot be excluded if the conversion of NO into NO2- and NO3- involves intermediary formation of the NO2 radical.(ABSTRACT TRUNCATED AT 250 WORDS)

Biotransformation↗
PubMed1991

Nitrosamine activation and detoxication through free radicals and their derived cations.

The enzymatic activation of simple dialkylnitrosamines is widely perceived to involve cytochrome P450-mediated alpha-hydroxylation to generate an unstable alpha-hydroxynitrosamine. This process can also result in the denitrosation of the nitrosamine, presumably through a common intermediate. We present evidence that the critical intermediate is the alkynitrosaminomethyl free radical, which we generated by thermal decomposition of a nitrosamino acid perester. The radical rapidly loses NO to generate an N-alkylmethyleneimine. The radical is also produced during the Ce(IV) oxidation of beta-hydroxynitrosamines after fragmentation, where it not only loses NO but is oxidized further to a cation which reacts with water to form an alpha-hydroxynitrosamine. These results provide models of the activation and detoxication pathways for beta-oxidized nitrosamines.

Biotransformation↗
PubMed1991

Localization of DNA adducts formed in the nasal cavity of the rat by the tobacco-specific nitrosamine 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK).

The tissue localization of the DNA adducts O6- and 7-methylguanine induced in the nasal cavity by the nicotine-derived carcinogen 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK, 30 mg/kg intraperitoneally) has been investigated immunocytochemically in male Sprague-Dawley rats. Adduct-specific nuclear staining, indicative of the metabolic activation of NNK to a methylating compound, was observed in both respiratory and olfactory mucosa. In the respiratory epithelium, strong staining was generally observed in areas devoid of goblet cells. Less intense staining was observed both in the serous gland cells and their efferent ducts in the respiratory submucosa, whereas the mucous gland cells were unstained. In the olfactory mucosa, the sustentacular and basal cells of the olfactory epithelium were moderately stained; staining varied substantially from site to site. No DNA adduct was detected in the olfactory cells. Strong nuclear staining, similar to that in the respiratory mucosa, was observed in the cells of the Bowman glands of the olfactory submucosa. A similar distribution of methylated DNA bases in nasal tissues has been observed in rats after exposure to other N-nitrosamines and in Syrian hamsters after exposure to NNK. This finding may indicate that in man the same cell types undergo DNA adduct formation after exposure to NNK and other N-nitrosamines.

Animals↗
PubMed1991

Some approaches to prevention of endogenous formation of N-nitrosamines in humans.

In a series of experiments on formation of N-nitrosamines from precursors in the gastric juice, we investigated individual nitrosation capacity and the influence of inhibitors on this process. In the presence of a molar ratio of 2:1 ascorbic acid:NaNO2, we found increased nitrosamine formation in 34% of gastric juice samples. Ferulic acid and caffeic acid generally suppressed nitrosation at high concentrations and stimulated it at low concentrations. The concentration at which the transition from a stimulating to an inhibitory effect occurs depends on individual differences in the gastric juice.

Antioxidants↗
PubMed1991

Hemoglobin adducts as biomarkers of exposure to and metabolic activation of carcinogenic tobacco-specific nitrosamines.

The carcinogenic tobacco-specific nitrosamines N'-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) form hemoglobin adducts in laboratory animals and humans. These adducts release 4-hydroxy-1-(3-pyridyl)-1-butanone (HPB) upon mild base hydrolysis. HPB released from human hemoglobin can be quantified by gas chromatography-mass spectrometry. It is the only available biochemical marker for determination of exposure to, and metabolic activation of, carcinogens present only in tobacco. Levels of HPB were highest in snuff-dippers, followed by smokers and nonsmokers. Large interindividual variations in adduct levels were observed. The relationship between HPB levels in globin and DNA of rats treated with NNK has been investigated in order to aid in interpretation of the data from humans. These studies have provided the initial database for understanding the metabolic activation of tobacco-specific nitrosamines in humans.

Animals↗
PubMed1990

[Effects of nitrosamine on in vitro cultured human esophageal epithelial cells].

Explant-cell culture system of human esophageal mucosa was used for studying the in vitro biological effects of nitrosamines, the major suspected causative agents of esophageal cancer in Linxian County, on esophageal epithelial cells. These carcinogens showed a cytotoxic effect in most of the 10 cases tested. A dose-response relationship of cell number reduction was observed at certain dose range. However, the effect of these carcinogens on cellular DNA synthesis was not always suppressive. At certain concentrations, nitrosamines mainly stimulated DNA synthesis in all of the 4 cases studied. The cells treated by these carcinogens seemed to have an enhanced growth potential during subculturing.

Adult↗
PubMed1975

Stability of nitrosamines in samples of lake water, soil, and sewage.

N-nitrosodimethylamine, N-nitrosodiethylamine, and N-nitrosodi-n-propylamine were resistant to degradation in soil, sewage, and lake water. No degradation of these nitrosamines was observed in lake water during a 3.5-month period. A lag of nearly 30 days occurred before their slow disappearance from soil; they disappeared slowly from sewage, but a minimum of 50% remained after 14 days. The results with sewage and soil suggesta a microbial involvement in the slow decomposition of these nitrosamines.

Biodegradation, Environmental↗
PubMedDate not supplied

[The effect of thiamine, riboflavin, nicotinamide and ascorbic acid on the formation of nitrosamines in meat products].

The data are presented on the content of nitrosamines in meat products prepared according to traditional technology versus the use of water-soluble vitamins and their complex. It is shown that the enrichment of sausage products and canned meat with thiamine, riboflavin, nicotinamide and ascorbic acid is conducive to better hygienic parameters of the products, with lower content of nitrosamines (from 29.4 to 72.6%) as compared to meat products prepared according to the traditional technology.

Ascorbic Acid↗
PubMed1978

Alpha-tocopherol: uses in preventing nitrosamine formation.

alpha-Tocopherol has been evaluated as a nitrite scavenger for the prevention of nitrosamine formation in a model system and under practical conditions. alpha-Tocopherol was found to react with nitrosating agents in both lipophilic and aqueous environments. The use of alpha-tocopherol was shown to inhibit aminopyrene-nitrite induced hepatotoxicity in rats and to reduce the amount of NDMA formed in cigarette smoke. Of primary interest is the finding of a significant reduction of NPYR formation in fried bacon. Nitrosamine inhibition was greater with alpha-tocopherol used in combination with sodium ascorbate than with sodium ascorbate alone.

Animals↗
PubMed1978

Preliminary observations on amines and nitrosamines in non-normal human gastric contents.

Gastric contents from fasting humans were pooled and analysed for amines. Volatile amines present were dimethylamine, trimethylamine and histamine; non-volatile amines found were cadaverine, putrescine, ethanolamine and tryptamine. Gastric contents from 35 patients, some before and/or after gastric stimulation with histamine or pentagastrin, were analysed for nitrosamines. N-Nitrosodiethylamine (NDEA) (5-30 microgram/kg) was present in four samples, N-nitrosodimethylamine (NDMA) (2 microgram/kg) in two samples and N-nitrosopyrrolidine (NPYR) (6 microgram/kg) in one sample. pH, nitrite and nitrate determinations were made on some samples. Medical diagnosis of patients could not be correlated with the presence of nitrosamines in the gastric contents.

Amines↗
PubMed1977

Mutagenicity of N-butyl-N-(4-hydroxybutyl)nitrosamine, a bladder carcinogen, and related compounds.

N-Butyl-N-(4-hydroxybutyl)nitrosamine (BBN), which specifically induces bladder tumors, was shown to be mutagenic to Salmonella typhimurium strains TA 1535 and TA100 in the presence of an S-9 mix prepared from the liver of rats treated with polychlorinated biphenyl. Reduced nicotinamide adenine dinucleotide was a more effective cofactor than reduced nicotinamide adenine dinucleotide phosphate in the activation of BBN by the rat liver S-9 fraction, N-Butyl-N-(3-carboxypropyl)nitrosamine, reported to be the main urinary metabolite of BBN as well as of N,N-dibutylnitrosamine and to induce urinary bladder tumors specifically, was found to be mutagenic without metabolic activation by the S-9 mix. The mutagenicities of 31 compounds related structurally or metabolically to BBN and N,N-dibutylnitrosamine were tested. Of these compounds, 13 have previously been demonstrated to be carcinogenic, and nine have been shown to be noncarcinogenic. All the carcinogenic compounds were found to be mutagenic to strain TA1535 with or without the S-9 mix. Four of the nine noncarcinogenic compounds were also mutagenic. These "false-positive" compounds were predicted, in fact, to be carcinogenic.

Animals↗
PubMed1988

Approaches to the development of assays for interaction of tobacco-specific nitrosamines with haemoglobin and DNA.

The tobacco-specific, nicotine-derived nitrosamines 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN) are among the most important carcinogens in tobacco and tobacco smoke. Treatment of Fischer 344 rats with these carcinogens resulted in alkylation of haemoglobin and DNA by the 4-(3-pyridyl)-4-oxobutyl group formed during their metabolism. This alkyl group can be detached from globin or DNA under mild hydrolytic conditions as 4-hydroxy-1-(3-pyridyl)-1-butanone, which appears to be a potentially useful dosimeter for human exposure to, and activation of, tobacco-specific nitrosamines.

Animals↗