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PubMed1990

Intestinal first-pass metabolism of nitrosamines. 4. Metabolism of N-nitrosodibutylamine in vascularly autoperfused jejunal and ileal loops of rats.

N-Nitrosodi-[1-14C]butylamine (NDBA) has been shown to undergo a high first-pass metabolism in isolated perfused rat small intestinal segments. Metabolites resulting from omega-hydroxylation of NDBA, the bladder carcinogens N-nitrosobutyl-(4-hydroxybutyl)amine (NB4HBA) and N-nitrosobutyl-(3-carboxypropyl)-amine (NB3CPA), accounted for greater than 90% of the total radioactivity absorbed. In the present study using vascularly perfused rat small intestinal segments, the high first-pass metabolism of NDBA could be confirmed under near in vivo conditions despite the much higher absorption rate. At the end of the 36 min experimental period 70-80% of the dose have been absorbed via the portal blood as opposed to 1-10% of the dose after 2 h in vitro perfusion. omega-Hydroxylation was again the most important metabolic pathway. However, the relationship of NB3CPA to NB4HBA was shifted in favor of NB4HBA, indicating a concentration and absorption rate dependency in the further metabolism of NB4HBA to NB3CPA.

Animals↗
PubMed1991

Mutational specificities of environmental carcinogens in the lacI gene of Escherichia coli: IV. The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone.

We have determined the mutational specificity of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) by the characterization of 58 induced Escherichia coli lacI-d mutants at the DNA sequence level. Metabolic activation of NNK was carried out using the S9 fraction from Aroclor 1254-treated rats. G:C----A:T transitions dominated the spectrum, accounting for 55% of the mutations recovered. The other base substitutions recovered include three A:T----G:C transitions as well as two A:T----T:A, three A:T----C:G, five G:C----C:G and five G:C----T:A transversions. Other classes of mutational events included two deletions, three duplications and three frame-shifts. The complexity of the NNK mutational spectrum appears consistent with a model that this compound induces mutations by both the methylation and the pyridoloxobutylation of DNA.

Bacterial Proteins↗
PubMed1991

Protective effects of vitamin A against the genotoxicity of NNK, a nicotine-derived N-nitrosamine.

In this investigation, the effect of vitamin A on 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induced genotoxic damage in rat liver was studied and correlated with NNK metabolism and DNA single strand breaks (DNA-SSBs). Male adult Fischer rats were fed a vitamin A deficient diet for 8 weeks and then divided into two sub-groups. Rats in group Ia and group Ib were fed vitamin A supplemented and vitamin A deficient diets respectively for an additional 4 weeks. Rats were then treated with a single i.p. injection of NNK (25-100 mg/kg) and subjected to partial hepatectomy 1 week later. After 72 h, liver perfusions were performed for cell preparation. Non-hepatectomized rats were used as controls (group IIa and IIb, consisting of rats fed vitamin A supplemented and deficient diets respectively). In non-hepatectomized rats (groups IIa and IIb), micronucleus (MN) frequencies were not significantly increased. This confirms the importance of cell proliferation for MN formation. In rats fed a vitamin A deficient diet and subjected to partial hepatectomy (group Ib), a significant increase of MN was observed (2.2 +/- 0.3, 5.7 +/- 0.9, 12.8 +/- 3.8 and 21.2 +/- 4.3% for control, 25, 50 and 100 mg NNK/kg body wt respectively). In rats fed a vitamin A supplemented diet (group Ia) we have observed a significant decrease of MN induction, as compared to rats fed a vitamin A deficient diet (group Ib) (2.7 +/- 1.0, 2.9 +/- 0.9, 9.7 +/- 2.7, 14.8 +/- 3.2% for control, 25, 50 and 100 mg NNK/kg body wt respectively). Freshly isolated hepatocytes from rats fed vitamin A deficient and supplemented diets but without NNK treatment in vivo were used to study NNK metabolism and DNA-SSBs. Results showed that hepatocytes isolated from rats fed a vitamin A supplemented diet (group C) metabolized NNK less effectively than hepatocytes isolated from rats fed a vitamin A deficient diet (group B) (NNK metabolism was decreased by 0.5-fold in group C as compared to group B). This inhibition was observed only with the NNK activation pathway, alpha-carbon hydroxylation, but not with a deactivation pathway: pyridine-N-oxidation. DNA-SSBs induced by NNK were also reduced in hepatocytes isolated from rats fed a vitamin A supplemented diet as compared to hepatocytes isolated from rats fed a deficient diet. These reductions were 7.8, 12.4 and 4.5% after 6 h of elution and 9.1, 8.5 and 3.0% after 9 h of elution for 1, 5 and 10 mM NNK respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Effect of phenethyl isothiocyanate on the metabolism of tobacco-specific nitrosamines by cultured rat oral tissue.

The effect of phenethyl isothiocyanate (PEITC) on the metabolism of N'-nitrosonornicotine (NNN) and 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) by cultured rat oral tissue was investigated. Two protocols were used. In one, oral tissue from untreated rats was cultured in the presence of 10 or 50 microM PEITC and either NNN or NNK. The levels of NNN and NNK metabolites released into the culture media were determined by HPLC analysis. The presence of 10 microM PEITC inhibited the formation of all NNN metabolites from 45 to 70% when the concentration of NNN was 1 microM or 10 microM. When the concentration of PEITC was 50 microM the extent of inhibition was from 70 to 90%. alpha-Hydroxylation of NNK was inhibited 70 to 90% and N-oxidation of NNK was inhibited 80 to 90% by 10 microM PEITC. Carbonyl reduction of NNK to NNAL was unaffected by 10 microM PEITC and only slightly inhibited by 50 microM PEITC. In the second protocol, rats were fed NIH-07 diet containing 3 mumol PEITC/g for 1-14 days. The metabolism of NNN by cultured oral tissue from these rats was decreased from 40 to 90% relative to that by tissue from control rats. NNK metabolism was inhibited 40 to 60%. The extent of inhibition was the same when rats were fed PEITC containing diet for 1 or 14 days. NNN and NNK are the only tobacco constituents which induce oral cavity cancer in an animal model. The results of this study suggest the possibility that PEITC may be useful as a chemopreventive agent for oral cavity cancer.

Animals↗
PubMed1992

Effects of phenethyl isothiocyanate, a carcinogenesis inhibitor, on xenobiotic-metabolizing enzymes and nitrosamine metabolism in rats.

Phenethyl isothiocyanate (PEITC), a constituent of cruciferous vegetables, has been shown to inhibit chemical carcinogenesis, possibly due to its ability to block the activation or to enhance the detoxification of chemical carcinogens. The present study was conducted to elucidate the biochemical mechanisms involved by characterizing the effects of PEITC on phase I and phase II xenobiotic-metabolizing enzymes. A single dose of PEITC to F344 rats (1 mmol/kg) decreased the liver N-nitrosodimethylamine demethylase (NDMAd) activity (mainly due to P450 2E1) by 80% at 2 h and the activity of NDMAd remained decreased by 40% at 48 h after treatment. The liver pentoxyresorufin O-dealkylase (PROD) activity and P450 2B1 protein level were elevated 10- and 7-fold at 24 h after treatment respectively. The liver microsomal ethoxyresorufin O-dealkylase (EROD) (mainly due to P450 1A) and erythromycin N-demethylase (mainly due to P450 3A) activities were decreased at 2-12 h after treatment and recovered afterwards. The lung microsomal PROD and EROD activities were not significantly affected; whereas, the nasal microsomal PROD and EROD activities were decreased by 40-50%. After a treatment with PEITC, the rates of oxidative metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were decreased in liver microsomes by 40-60% at 2 h and recovered gradually; the rates in lung microsomes were markedly decreased by 60-70% at 2 h and remained at the decreased level at 24 h; and the rates in nasal mucosa microsomes were decreased gradually with the lowest activities observed at 18 h (50%) followed by a gradual recovery. Furthermore, the treatment with PEITC resulted in a maximal 5-fold increase of NAD(P)H:quinone oxidoreductase and 1.5-fold increase of glutathione S-transferase activities in the liver, but the activities of these two enzymes were not significantly affected in the lung and nasal mucosa. The sulfotransferase activity in the liver was decreased by 32-48% at 24-48 h after treatment; the nasal activity was increased by 1.8- to 2.5-fold, but the lung activity was not significantly changed. The hepatic UDP glucuronosyltransferase activity was slightly decreased at 2 h but slightly increased at 48 h after treatment, but no changes were observed for the lung and nasal activities. The study demonstrates that PEITC selectively affects xenobiotic-metabolizing enzymes in the liver, lung and nasal mucosa and it is especially effective in inhibiting the P450-dependent oxidation of NNK in the lung and of NDMA in the liver.

Animals↗
PubMed1993

Production of scatter factor-like activity by a nitrosamine-induced pancreatic cancer cell line.

Two hamster pancreatic cancer cell lines, PC-1 and PC1.0, established from N-nitrosobis(2-oxopropyl)amine-induced pancreatic ductal/ductular adenocarcinomas exhibit different growth patterns. PC-1 cells, which produce well differentiated adenocarcinomas in vitro after allogeneic inoculation, form cell aggregates and characteristic island-like structures in vitro. PC1.0 cells, which produce poorly differentiated tumors in vivo, form dispersed colonies in vitro. Conditioned medium prepared from PC1.0 cells inhibits PC-1 cells from forming island-like colonies. The conditioned medium also prevents several human pancreatic carcinoma cell lines, HPAF, CD11 and CD18, from forming compact colonies. These properties are similar to those described previously as scatter factors. The scatter factor-like activity is heat-labile, acid-stable, non-dialyzable, trypsin sensitive and unaffected by reducing agents. The activity is not suppressed by addition of heparin, and it does not bind to heparin. In addition, the scatter phenomenon is not reproduced by acidic or basic fibroblast growth factor, epidermal growth factor or transforming growth factor-beta 1. Based on these findings, it appears that the scattering activity produced by PC1.0 cells differs from the scatter factors that have been identified in other systems.

Adenocarcinoma↗
PubMed1994

Increased nitrosamine and nitrate biosynthesis mediated by nitric oxide synthase induced in hamsters infected with liver fluke (Opisthorchis viverrini).

We previously reported that increased endogenous nitrosation in human subjects infected with the liver fluke Opisthorchis viverrini in north-east Thailand could be a risk factor for the development of cholangiocarcinoma. In the present study we examined our hypothesis that this increased endogenous nitrosation is mediated by nitric oxide (NO) synthase induced by O. viverrini infestation. Syrian golden hamsters experimentally infected with O. viverrini liver fluke excreted in the urine significantly greater amounts of nitrate, a stable oxidization product of NO, than untreated hamsters (3.64 +/- 0.86 versus 2.64 +/- 0.60 mumol/hamster/day, P < 0.001). When the rapidly nitrosatable thiazolidine 4-carboxylic acid was administered orally, the infected hamsters also excreted significantly elevated levels of N-nitrosothiazolidine 4-carboxylic acid than untreated hamsters (4.27 +/- 2.20 versus 2.33 +/- 1.13 nmol/hamster/day, P < 0.01), indicating that endogenous nitrosation is elevated in the animals with liver fluke. NO synthase activity measured in liver cytosol was about twice as high in the infected hamsters as in untreated animals. The enzyme, whose biochemical characteristics were similar to that induced in activated murine macrophages, was immunohistochemically localized in the cytoplasm of macrophages and eosinophils in the inflammation zone surrounding the parasite-containing bile ducts. These results support our hypothesis that, in fluke-infected subjects, NO synthase induction leads to excess production of NO and the observed elevated endogenous nitrosation. Since high concentrations of NO exert cytotoxic and mutagenic effects per se, excess NO produced in chronically infected/inflamed tissues may also play a role in initiation and subsequent modulation stages of cholangiocarcinoma development.

Amino Acid Oxidoreductases↗
PubMed1997

Genetic alterations in N-bis(2-hydroxypropyl)nitrosamine-induced rat transplantable thyroid carcinoma lines: analysis of the TSH-R, G(alpha)s, ras and p53 genes.

It has recently been shown that point mutations of the TSH-R or G(alpha)s genes are associated with autonomous hyperfunctioning thyroid adenomas and differentiated carcinomas. We therefore screened for mutations in the TSH-R, G(alpha)s, ras and p53 genes in nine rat transplantable thyroid carcinoma lines derived from tumors induced by DHPN as a chemical carcinogen. Mutations were identified using single-strand conformation polymorphism and DNA sequencing analysis. Point mutations in G(alpha)s codon 201 (CGC-->CAC) were detected in three lines (33%), resulting in a heterozygous alteration (Arg-->His) in the expressed G(alpha)s protein. The mean intracellular cAMP level (2.30 +/- 0.27 nmol/mg) of the three mutated cell lines was significantly increased as compared with that of the lines (1.54 +/- 0.32 nmol/mg) without the G(alpha)s mutation (P < 0.01, by paired t-test). Also, these three cell lines had an activating mutation in Ki-ras codon 12 (GGT-->GAT). One TSH-R gene mutation was found with a base substitution in codon 636 (TGC-->TGT) but no amino acid change. No p53 gene (exons 5-8) mutations were detected in any of the cell lines analyzed. The results suggest that mutational activation of the G(alpha)s gene may play a tumorigenic role through constitutive activation of the cAMP pathway and that G-->A point mutations in the G(alpha)s and ras genes in thyroid carcinomas directly reflect interaction of the chemical carcinogen with guanine residues in DNA.

Animals↗
PubMed1981

Biological and chemical studies involving methyl-t-butylnitrosamine, a non-carcinogenic nitrosamine.

Methyl-t-butylnitrosamine (MtBN) was tested for carcinogenicity by s.c. injection in the Syrian golden hamster. No tumors were observed at 160, 80 or 40 mg/kg/week, in accord with Druckrey's report that ethyl-t-butylnitrosamine (EtBN), the homolog of MtBN, was not carcinogenic in the rat. Acetoxymethyl-t-butylnitrosamine, an activated form of MtBN, was also chronically tested by s.c. injection and found to be non-carcinogenic. It was demonstrated that 2-methylpropane diazotic acid, the proposed "ultimate" reactive metabolite of MtBN, afforded the carbenium ion product t-butyl alcohol in 63% yield. These results are consistent with the hypothesis that MtBN and EtBN are not carcinogenic because the proposed "ultimate" metabolite in their metabolic activation cannot interact with the critical cellular site due to steric reasons.

Animals↗
PubMed2001

Increased susceptibility of poly(ADP-ribose) polymerase-1 knockout mice to nitrosamine carcinogenicity.

The involvement of poly(ADP-ribose) polymerase-1 (Parp-1), one of the poly(ADP-ribose) polymerase family proteins, in genomic stability, DNA repair and cell death triggered by DNA damage has been well documented. However, the potential role of Parp-1 in carcinogenesis has not been well evaluated. In this study the carcinogenic activity of N:-nitrosobis(2-hydroxypropyl)amine (BHP) was studied in Parp-1(-/-) mice, generated by disrupting P:arp-1 gene exon 1. Parp-1(-/-) and Parp-1(+/+) male mice received 0, 250 and 500 p.p.m. BHP in their drinking water for 20 weeks and were then killed. The percentage of animals bearing hemangiomas and hemangiosarcomas in the liver and numbers of tumors per mouse were markedly higher in the Parp-1(-/-) groups given 250 or 500 p.p.m. BHP than in their Parp-1(+/+) counterparts. Hemangiosarcomas developed only in Parp-1(-/-) mice. In the lung the numbers of adenomas per mouse were increased in Parp-1(-/-) mice given BHP at 250 and 500 p.p.m. (P < 0.01) compared with the Parp-1(+/+) case. The results show that susceptibility to BHP is significantly elevated in Parp-1(-/-) mice, thus providing direct evidence that Parp-1 is relevant to carcinogenesis.

Adenocarcinoma↗
PubMed2001

Human cervical tissue metabolizes the tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, via alpha-hydroxylation and carbonyl reduction pathways.

We determined the ability of human epithelial cervical cells, human cervical microsomes and cytosol to metabolize 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). All preparations metabolized NNK by alpha-hydroxylation, demonstrated by the presence of 4-oxo-4-(3-pyridyl)butyric acid (keto acid), and by carbonyl reduction, illustrated by the formation of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL). Cervical cells metabolized NNK by the oxidative pathway to an extent comparable to that by the reductive pathway. In both human cervical cytosol and microsomes, the concentration of alpha-hydroxylation products ranged from undetectable to 10 times lower than those of NNAL. An apparent K(m) and V(max) of 7075 microM and 650 pmol/mg/min, respectively, were determined for the keto acid in one microsomal preparation. NNAL was formed in all preparations at the highest levels, ranging from 16.9 to 35.5 pmol/10(6) cells in incubations with ectocervical cells and 6.2 pmol/10(6) cells in incubations with endocervical cells. NNAL levels were 1.88-4.95 and 1.44-2.08 pmol/mg/min in human cervical microsomes and cytosolic fractions, respectively. An apparent K(m) of 739 microM and a V(max) of 1395 pmol/mg/min for NNAL formation were established in the same microsomal preparation used for the keto acid kinetics study. The stereochemistry of the NNAL formed in incubations of NNK with human cervical cells and subcellular fractions was determined by derivatization with (S)-(-)-methylbenzyl isocyanate. Human cervical cells and microsomes both formed the (R)-enantiomer of NNAL almost exclusively; incubations with human cervical cytosol resulted predominantly in the formation of the (S)-enantiomer. Substrates for 11 beta-hydroxysteroid dehydrogenase, cortisone, glycyrrhizic acid and metyrapone all inhibited the formation of NNAL in incubations with human cervical microsomes; the inhibition ranged from 16% to 80%. These studies illustrate that human cervical tissue can metabolize NNK by both oxidative and reductive pathways and that 11 beta-HSD may, in part, be responsible for the carbonyl reduction of NNK.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1982

Fluoro-substituted N-nitrosamines. 5. Carcinogenicity of n-nitroso-bis-(4,4,4-trifluoro-n-butyl)amine in rats.

N-Nitroso-bis-(4,4,4-trifluoro-n-butyl)amine (F-6-NDBA) has been synthesized as a derivative of the rat urinary bladder carcinogen N-nitrosodibutylamine (NDBA). Its chronic administration by gavage to Sprague-Dawley rats induced a significant incidence of malignant tumors of the liver and the lungs. Tumors in the liver were diagnosed as multifocal hepatocellular carcinomas and those of the lungs were mainly squamous cell carcinomas. No tumors were observed in the urinary bladder. This confirms earlier results from metabolism and animal carcinogenicity experiments indicating the importance of metabolic oxidation at the terminal carbon atom of NDBA for its organ-specific effects. This metabolic omega-oxidation is blocked in F-6-NDBA.

Animals↗
PubMed1982

Fluoro-substituted N-nitrosamines. 4. Comparative genotoxic activities of N-nitrosodibutylamine and three fluorinated analogues in two bacterial systems.

N-Nitrosodibutylamine (NDBA) and three fluorinated analogues (N-nitroso (4,4,4-trifluorobutyl-amine, F3NDBA; N-nitrosobis (4,4,4-trifluorobutyl)amine, F6NDBA; and N-nitrosobis (2,2,3,3,4,4,4-heptafluorobutyl) amine, F14NDBA were comparatively investigated for biological activity in two bacterial systems. Opposite orders of magnitude were obtained for their potency in the two tests. For inducing his+ reversion in auxotrophic strains of Salmonella typhimurium the sequence was F3NDBA greater than F6NDBA greater than NDBA and for inducing lethal DNA damage in repair deficient strains of Escherichia coli WP2 it was NDBA greater than F6NDBA. F14NDBA was not active in either test system.

Animals↗
PubMed1984

Carcinogenesis in rats by some hydroxylated acyclic nitrosamines.

A comparison was made of the carcinogenic effectiveness of five hydroxylated nitrosodialkylamines given to female F344 rats in drinking water. Nitroso-2,3-dihydroxypropyl-2-hydroxypropylamine was the most potent carcinogen among those examined, and induced almost exclusively tumors of the upper gastrointestinal tract. Considerably less potent was nitrosobis-(2-hydroxypropyl)amine, which also induced mainly tumors of the esophagus, although several animals also had tumors of the nasal cavity. Nitrosodiethanolamine was weaker again, and induced a high incidence of hepatocellular carcinomas. Nitroso-2-hydroxypropylethanolamine, which can be considered a hybrid of nitrosodiethanolamine, and the bis-hydroxypropyl compound, induced both esophageal tumors and hepatocellular carcinomas, together with some liver angiosarcomas; it appeared to lie in potency between the two symmetrical compounds. In contrast, nitroso-2,3-dihydroxypropylethanolamine was a very weak carcinogen, having little life-shortening effect; it induced hepatocellular carcinomas in only a small number of animals, together with some neoplastic nodules.

Animals↗
PubMed1985

Metabolism and tissue distribution of tobacco-specific N-nitrosamines in the marmoset monkey (Callithrix jacchus).

Three male marmoset monkeys (Callithrix jacchus) were injected i.v. with the tobacco-specific carcinogen [2'-14C]N'-nitrosonornicotine (NNN) (20.3 mumol/kg body weight) or [carbonyl-14C]4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (18.8 or 420 mumol/kg body weight). They were sacrificed 4 h later. Tissue distribution was studied in two monkeys by whole-body autoradiography and by computer-assisted densitometric analysis of the autoradiograms. The autoradiograms showed a high level of radioactivity in the liver, nasal mucosa, kidneys, melanin of the eyes, hair-follicles of the skin and in the ceruminous ear glands of the monkeys. Total level of radioactivity was 5.7 times higher in the liver of the [carbonyl-14C]NNK-injected monkey than in that of [2'-14C]-NNN-injected monkey. Washing the sections with trichloroacetic acid and organic solvents selectively removed free metabolites leaving metabolites bound to cellular macromolecules. Level of bound metabolites was 1.5 times higher in the nasal mucosa than in the liver of the [2'-14C]NNN monkey. Levels of bound metabolites were similar in the liver of NNN- and NNK-treated monkeys. The results indicate that the liver and nasal mucosa of C. jacchus can activate NNN and NNK to alkylating species. Unbound metabolites present in the liver, lung, kidneys, eye, blood and urine were extracted and separated by h.p.l.c. Hydroxylation of the carbons alpha to the N-nitroso group of NNN were the major metabolic pathways. Unmetabolized NNN was the major radioactive component in the liver, lung, eye and blood. Reduction of the carbonyl of NNK yields 4-(methylnitrosamino)-1-(3-pyridyl)butan-1-ol (NNAl). NNAl was present in all tissues analyzed and was the major radioactive component in the eye and stomach lumen. It was also excreted in the urine. NNK and NNAl were metabolized by alpha-carbon hydroxylation. These results suggest that in C. jacchus, NNN, NNK and NNAl are activated to alkylating species by alpha-carbon hydroxylation. In the third monkey injected with NNK, DNA methylation was observed in the liver and nasal mucosa but not in the lung and kidneys. Pulmonary tissues of C. jacchus, unlike those of F344 rats, do not have the enzymic capacities to activate NNK to methylating species.

Animals↗
PubMed1985

Screening of microorganisms for nitrosation catalysis at pH 7 and kinetic studies on nitrosamine formation from secondary amines by E. coli strains.

Thirty-eight strains of microorganisms isolated from infected human trachea, urine, blood and faeces were examined for their ability to form N-nitrosomorpholine from morpholine and nitrite at pH 7.25. Twenty-five bacterial strains exhibited nitrosation activity, including 18 out of 19 strains of Escherichia coli and three out of nine Pseudomonas aeruginosa, Proteus morganii, Proteus mirabilis, Klebsiella pneumoniae and Neisseria strains; E. coli A10 strain showed the highest activity. Formation of N-nitrosomorpholine was proportional to the incubation time up to 2 h and to the number of resting E. coli A10 cells; the reaction followed Michaelis-Menten kinetics. Nitrosation rate appeared to be dependent on the pKa value of several amines studied. As the nitrosation catalysis was heat-labile, our data suggest that N-nitrosation is catalysed by a bacterial enzyme(s). This reaction may lead to enhanced endogenous nitrosation in subjects suffering from an achlorhydric stomach or from chronic urinary tract infections.

Amines↗
PubMed1986

N-nitrosamines and Nigerian habitual drinks, and cancer.

Commercially available samples of Nigerian lager beers and bottled palm wine, and of root cuttings of medicinal plants, assayed for volatile N-nitroso compounds and nitrosatable entities, respectively, by chromatographic, chemiluminescence, colorimetric, derivatisation and nitrosation methods, contained nitrosodimethylamine (0.2-2.3 micrograms/kg; mean, 0.9 micrograms/kg) only in the drinks, and dimethylamine (DMA) and piperidine (1 mg/kg as DMA) in the roots.

Beer↗