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PubMed1996

Pyruvate dehydrogenase complex-catalyzed formation of N-arylacetohydroxamic acids from nitroso aromatic compounds in rat isolated cells and perfused organs.

The formation of N-arylacetohydroxamic acid derivatives from m-nitrosobenzyl alcohol (MBNO) and a nitroso derivative of chloramphenicol, 2,2-dichloro-N-[2-hydroxy-1-(hydroxymethyl)-2-(4-nitrosophenyl) ethyl]acetamide, in the presence of pyruvate was investigated with rat isolated cells (heart, kidney, liver, small intestine, lung, bone marrow and spermatozoa) and perfused organs (liver and heart). The activity in N-(m-hydroxymethylphenyl) acetohydroxamic acid (MBHA) formation was found in all the cells tested. Measurement of the kinetic parameters revealed that K(m) values of MBNO were ca. 0.3 mM and that the order of Vmax per cell was heart > kidney > liver > small intestine. In the hepatocytes, MBHA was metabolized further and the in vitro intrinsic clearance of MBHA was 1.91 +/- 0.24 ml/min/10(8) cells. In a single-pass perfusion of rat liver with MBNO, the corresponding amino, acetylamino and azoxy derivatives and unknown materials were formed in addition to MBHA. The activity in MBHA formation was increased by the addition of both diethyl maleate and paraoxon. In a recirculating perfusion of rat liver with MBNO, however, the net MBHA formation was hardly detected, because of the disposition of MBHA formed. The hepatic clearance of MBHA was 1.15 +/- 0.06 ml/min/g of liver. In a recirculating perfusion of isolated rat heart with MBNO, MBHA was formed as a major metabolite and further biotransformation was not found. The N-arylacetohydroxamic acid derivative of 2,2-dichloro-N-[2-hydroxy-1-(hydroxymethyl)-2-(4-nitrosophenyl) ethyl]acetamide was also formed in rat bone marrow cells and the isolated perfused heart. These results indicate that the formation of N-arylacetohydroxamic acids from nitroso aromatic compounds and pyruvate catalyzed by pyruvate dehydrogenase complex proceeds in virtually all mammalian tissues.

Animals↗
PubMed1991

Organ-specific modification of tumor development by low-dose combinations of agents in a rat wide-spectrum carcinogenesis model.

The combined effects of low doses of various carcinogens and carcinogenesis modifiers on tumor development were investigated by using a wide-spectrum organ carcinogenesis model in F344 rats. These agents were administered as three groups: (1) a group of known hepatocarcinogens; (2) a group of nitroso compounds having various target organ specificities; and (3) a group of antioxidants having various inhibiting or enhancing activities depending on the target organ. Doses were used which were generally below the known effective level for the individual chemical. These groups of chemicals were administered with or without prior administration of N-diethylnitrosamine (100 mg/kg body wt., i.p.), N-methylnitrosourea (4 x 20 mg/kg body wt., i.p.) and dihydroxy-di-N-propylnitrosamine (0.1% in drinking water for 2 weeks). The hepatocarcinogen group in combination with various nitroso compounds increased the incidences of liver hyperplastic nodules and hepatocellular carcinomas. In contrast, incidences were clearly reduced when the hepatocarcinogens and/or the nitroso compounds were administered in combination with the antioxidants. For the urinary bladder, the combination with nitroso compounds and antioxidants enhanced cancer development, and the addition of hepatocarcinogens further increased tumorigenesis. For the glandular stomach, additive effects on the numbers of pepsinogen isozyme 1-altered pyloric glands, a putative preneoplastic lesion, were produced by the combination treatment of antioxidants and the nitroso compounds. No synergistic effects on tumor development were seen in other organs. The results of the present study demonstrated that combinations of various compounds at low doses can additively or synergistically exert either enhancing or inhibitory effects on the development of preneoplastic and neoplastic lesions in different organs in a single model having a wide spectrum of organ effects.

Animals↗
PubMed2002

Helicobacter pylori does not mediate the formation of carcinogenic N-nitrosamines.

BACKGROUND: Both N-nitroso compounds and colonization with Helicobacter pylori represent known risk-factors for the development of gastric cancer. Endogenous formation of N-nitroso compounds is thought to occur predominantly in acidic environments such as the stomach. At neutral pH, bacteria can catalyze the formation of N-nitroso compounds. Based on experiments with a noncarcinogenic N-nitroso compound as end product, and using only a single H. pylori strain, it was recently reported that H. pylori only displays a low nitrosation capacity. As H. pylori is a highly diverse bacterial species, it is reasonable to question the generality of this finding. In this study, several genetically distinct H. pylori strains are tested for their capacity to form carcinogenic N-nitrosamines. MATERIALS AND METHODS: Bacteria were grown in the presence of 0-1000 microM morpholine and nitrite (in a 1 : 1 molar ratio), at pH 7, 5 and 3. RESULTS: Incubation of Neisseria cinerea (positive control) with 500 microM morpholine and 500 microM nitrite, resulted in a significant increase in formation of N-nitrosomorpholine, but there was no significant induction of N-nitrosomorpholine formation by any of the H. pylori strains, at any of the three pH conditions. CONCLUSION: H. pylori does not induce formation of the carcinogenic N-nitrosomorpholine in vitro. The previously reported weak nitrosation capacity of H. pylori is not sufficient to nitrosate the more difficulty nitrosatable morpholine. This probably also holds true for other secondary amines. These results imply that the increased incidence of gastric cancer formation that is associated with gastric colonization by H. pylori is unlikely to result from the direct induced formation of carcinogenic nitrosamines by H. pylori. However, this has to be further confirmed in in vivo studies.

Antigens, Bacterial↗
PubMed2006

Evaluation of nitroreductase and acetyltransferase participation in N-nitrosodiethylamine genotoxicity.

N-Nitroso compounds, such as N-nitrosodiethylamine (NDEA), are a versatile group of chemical carcinogens, being suspected to be involved in gastrointestinal tumors in humans. The intestinal microflora can modify a wide range of environmental chemicals either directly or in the course of enterohepatic circulation. Nitroreductases from bacteria seem to have a wide spectrum of substrates, as observed by the reduction of several nitroaromatic compounds, but their capacity to metabolize N-nitroso compounds has not been described. To elucidate the participation of nitroreductase or acetyltransferase enzymes in the mutagenic activity of NDEA, the bacterial (reverse) mutation test was carried out with the strains YG1021 (nitroreductase overexpression), YG1024 (acetyltransferase overexpression), TA98NR (nitroreductase deficient), and TA98DNP6 (acetyltrasferase deficient), and YG1041, which overexpresses both enzymes. The presence of high levels of acetyltransferase may generate toxic compounds that must be eliminated by cellular processes or can lead to cell death, and consequently decrease the mutagenic effect, as can be observed by the comparison of strain TA98DNP6 with the strains TA98 and YG1024. The slope curves for TA98 strain were 0.66 rev/microM (R(2) = 0.51) and 52.8 rev/microM (R(2) = 0.88), in the absence and presence of S9 mix, respectively. For YG1024 strain, the slope curve, in the presence of S9 mix was 6897 rev/microM (R(2) = 0.78). Our data suggest that N-nitroso compounds need to be initially metabolized by enzymes such as cytochromes P450 to induce mutagenicity. Nitroreductase stimulates toxicity, while acetyltransferase stimulates mutagenicity, and nitroreductase can neutralize the mechanism of mutagenicity generating innoccuos compounds, probably by acting on the product generated after NDEA activation.

Acetyltransferases↗
PubMed1976

Nitrite, nitrosamines, and cancer.

Carcinogenic N-nitroso compounds are formed from the reaction of naturally-occurring amines and nitrites that may be added to foods or produced by bacterial reduction of nitrate. N-Nitroso compounds can be produced during processing, storage and preparation of foods and in the mammalian stomach. Factors that influence the rates of nitrosation reactions include pH, temperature, catalysts, and inhibitors. Predictions of the extent of nitrosation are complicated by these factors and ultimately the amounts and types of N-nitroso compounds present must be determined by direct analysis. Methods for detection and estimation of volatile nitrosamines are available and low levels (parts per billion) have been found in some cured meat and fish products. General methods for detection of all N-nitroso compounds are not available yet, but are under development. Evaluation of the risk to human populations from these compounds is difficult in the absence of more comprehensive data on their environmental distribution.

Animals↗
PubMedDate not supplied

Surveillance of preservatives and their interactions in foodstuffs.

The organization of food surveillance in the UK is described, in particular as it has been applied to preservatives and their interaction products in foods. Applications of nitrates and nitrites as preservatives are discussed, together with the consequential exposure of consumers to these anions and their reaction products. Analytical methods for the determination of volatile and non-volatile N-nitroso compounds are referred to in relation to the results in food surveillance studies. Concentrations of Apparent Total N-nitroso Compounds (ATNC) averaged 2900 micrograms(N-NO)/kg in fried smoked bacon compared with 2400 micrograms/kg in fried unsmoked bacon; of this, known volatile and non-volatile N-nitroso compounds accounted for only 10-20%. ATNC were not detected in cheeses except those manufactured with added nitrate when ATNC levels up to 210 micrograms(N-NO)/kg were detected. Further studies are needed to determine the identity and toxicological properties of the non-volatile N-nitroso compounds.

Food↗
PubMed1976

[Nitrosamines. Review].

Nitrosamines are an extremely carcinogenic class of compounds. The hasard, bound with the occurrence of this compounds in the food and the possibility to be formed in vivo, during the digestion, justifies the current works. The authors quoting numerous works on different laboratory's animals, remind the toxicity. and carcinogenicity of this compounds. The metabolism is also discussed. The N-nitroso, compounds may be formed in food from the presence of the precursors (nitrite or nitrate, amines and amino-acides). The synthesis takes place during the technological processes, the storage and the house cooking. Today, the marginal effect dose is estimated as 10 mug/kg of daily food. The carcinogenicity has not been demonstrated in human, but is strongly suspected. The amount of N-nitroso compounds in human food is generally low. Many factors can influence the reaction; it is inversely related to the basicity of secondary amine and optimum pH is around pH 4. A lot of compounds such as sodium ascorbate inhibit the synthesis in food. A number of recent reports using reliable methodology have identified nitrosamines at the lower part per billion level. Dimethyl-nitrosamines occurs, very sporadically in a number of cooked meat samples. The nitrosopyrrolidine appears frequently in fried but not in uncooked products. The nitrosopiperidine seems to be bind with the presence of pepper in food. Finally the presence of nitrosamides (nitrososarcosine) and nitrosoaminoacides (nitrosoproline, nitrosohydroxy-proline) is being quested. The N-nitroso compounds may be synthetized in vivo during the digestion at the acide medium of the stomach or by bacterial action during the transit in the gut...

Amino Acids↗
PubMed1990

Gastric nitrite processing in the surgically altered maximal and minimal bile reflux ferret model.

Ingested nitrate and nitrite have been shown to contribute to endogenous, N-nitroso compound formation in man and experimental animals. N-nitroso compounds have long been suspected of contributing to higher levels of gastric cancer in various populations. Reconstructive gastric surgery to treat ulcers is accompanied by a change in bile reflux, gastritis and an increased incidence of gastric cancer in humans. To evaluate possible connections between gastric nitrite processing, reconstructive surgery and gastric cancer, the surgically altered domestic ferret, Mustela putorius furo, was used as an experimental model. The aim of the study was to determine if surgery would alter the stomach in a way which would increase gastric nitrite concentration, and thereby enhance the likelihood of gastric N-nitroso compound formation. Three groups of ferrets, one control group (n = 6) and two groups of surgically altered ferrets, one to simulate maximal bile reflux (MABR, n = 6), and the other to model minimal bile reflux (MIBR, n = 7), were studied. Each group's response to an exogenously administered dose of sodium nitrite did not differ significantly with respect to rate of gastric nitrite absorption, with half-lives in the 13-min range. Permeability of gastric mucosa to nitrite did not differ between controls and MIBR ferrets. Mean doubling time of gastric nitrate appeared slowed in surgically altered ferrets. Mean rate of gastric emptying was the same in the three groups, but appeared delayed initially in MIBR ferrets. Thiocyanate concentrations, pH and HCl secretion, all parameters which have been shown to affect gastric nitrite processing, did not differ significantly between groups. Gastric mucosal endoscopic biopsies obtained at 6-month intervals showed no clear difference in degree of mucosal inflammation and/or dysplasia in the three groups. These findings indicate that gastric mucosal neoplasia has not occurred in this model and that changes in parameters favoring gastric N-nitrosation, even if relevant to the disease process, are not apparent at this time.

Animals↗
PubMed1984

Susceptibilities of drugs to nitrosation under standardized chemical conditions.

Of 22 drugs with either a N,N-dimethylamino, N,N-diethylamino or N-morpholino group in the molecule, eight were converted to volatile N-nitrosamines by nitrosative cleavage in reactions of nitrite and drug in a molar ratio of 4:1 at pH 3. Under standardized conditions yields were greatest with aminopyrine and minocycline which contains two N,N-dimethylamino groups in the molecule. Oxytetracycline, chlortetracycline, tetracycline, promethazine, chlorpromazine, imipramine and disulfiram gave much lower yields and amitriptyline, clomiphene, clomipramine, dextropropoxyphene, diphenhydramine, disopyramide, erythromycin, mepyramine, methapyrilene, penicillin G procaine salt, procaine, tamoxifen, trimeprazine and tripelennamine yielded no detectable levels of volatile N-nitrosamines. Nitrosation products of 57 drugs were also examined by a group selective procedure estimating both volatile and non-volatile N-nitroso compounds. Virtually all of the yield obtained from aminopyrine or minocycline could be accounted for by N-nitrosodimethylamine (NDMA). However, compounds yielding excess N-nitrosamines compared to NDMA were obtained from the other three tetracyclines, presumably as a result of the cleavage of a methyl group from the N,N-dimethylamino substituent to form desmethyl-N-nitroso compounds. In general, the drugs giving the highest yields of N-nitroso compounds were those containing secondary rather than tertiary amino groups. A considerable range of susceptibilities towards nitrous acid was observed overall; ten drugs containing a secondary or tertiary amino- or amido- or hydrazido - group did not react with nitrous acid to form N-nitroso compounds.

Chemical Phenomena↗
PubMed1993

Identification, synthesis and properties of 5-(aziridin-1-yl)-2-nitro-4-nitrosobenzamide, a novel DNA crosslinking agent derived from CB1954.

5-(Aziridin-1-yl)-4-hydroxylamino-2-nitrobenzamide, the active form of 5-(aziridin-1-yl)-2,4-dinitrobenzamide (CB1954), can react spontaneously with oxygen, and in aqueous solution yields 5-(aziridin-1-yl)-2-nitro-4-nitrosobenzamide and hydrogen peroxide. Mild biological reducing agents such as NAD(P)H, reduced thiols and ascorbic acid rapidly re-reduced the nitroso compound to the hydroxylamine. Both compounds were equally efficient at inducing cytotoxicity and DNA interstrand crosslinking in cells when exposed in phosphate-buffered saline (PBS). Neither agent was capable of inducing cross-links in isolated DNA. When acetyl coenzyme A was included in the incubation, crosslink formation was seen with the hydroxylamine, but not with the nitroso compound. Thus, the nitroso compound is acting as a prodrug for the hydroxylamine, and needs to be reduced to this compound to exert its cytotoxic effects. In vivo anti-tumour tests showed that neither compound was effective in its own right. This may be due to the rapid reduction of the nitroso to the hydroxylamine, and the reaction of the hydroxylamine with serum proteins. The chemical synthesis of the 5-(aziridin-1-yl)-2-nitro-4-nitrosobenzamide, and an improved synthesis of 5-(aziridin-1-yl)-4-hydroxylamino-2-nitrobenzamide is described. These results emphasize the potential efficacy of the in situ activation of prodrugs such as CB1954 either by endogenous enzymes such as DT diaphorase, or by antibody directed enzyme prodrug therapy (ADEPT).

Animals↗
PubMed1986

[Abnormal effect of nitrosation inhibitors in human gastric juice].

The paper discusses the effect of vitamins C and E and Plantaglucide on nitroso compounds yield in the course of nitrosation of amines in human gastric juice. The study group included 56 subjects. The above drugs capable of inhibiting in vitro nitrosation produced an anomalous effect in gastric juice of some subjects, i.e. potentiated nitroso compounds yield in nitrosation of amines by sodium nitrite. The said action of vitamins C and E was apparent in dimethylamine and amidopyrine nitrosation but it was not in morpholine nitrosation. Sharply increased levels in nitroso compounds were observed in some mice fed precursors of nitroso compounds in combination with vitamin C and Plantaglucide. These data point to an anomalous effect of the drugs on the body.

Animals↗
PubMed1987

Effect of histamine H2-receptor antagonist therapy on the mutagenic activity of gastric juice.

There is concern at present that treatment with histamine H2-receptor antagonists might promote the development of gastric cancer by producing conditions which favour intragastric formation of N-nitroso compounds. If H2-receptor antagonist therapy causes increased intragastric levels of N-nitroso compounds, an issue not yet resolved by analytical studies, corresponding changes in the mutagenic activity of gastric juice might be anticipated. In this study mutagenic activity and pH were measured in fasting gastric aspirate from 18 peptic ulcer patients before and during the final week of therapy with ranitidine (n = 10) or cimetidine (n = 8). Mutagenic activity was assessed using Salmonella typhimurium TA98 and TA100 in a modified pre-incubation "fluctuation" test. No significant change in mutagenic activity was detected after therapy. Of 15 patients found to have significant mutagenic activity in their fasting gastric juice before treatment, 14 remained mutagenic following treatment. Mutation frequencies (sum of positive wells in duplicate 96-well microtitre plates, mean +/- SD) for TA98 and TA100 were respectively, 20 +/- 34 and 100 +/- 64 before compared with 10 +/- 6 and 102 +/- 65 after therapy (p greater than 0.05). Changes in mutagenic activity were similar in both treatment groups and unrelated to duration of therapy, changes in gastric pH or ulcer healing. In vitro, neither cimetidine in aqueous solution, nor gastric juice preincubated with cimetidine showed significant mutagenic activity. These results provide no evidence that increased intragastric levels of genotoxic chemicals, such as N-nitroso compounds, occur during H2-receptor antagonist therapy.

Adult↗
PubMed1987

Bacterially catalysed N-nitrosation reactions and their relative importance in the human stomach.

Human exposure to endogenously formed N-nitroso compounds has frequently been suggested as a causative factor in carcinogenesis where this is related to chronic bacterial infection such as is seen in gastric achlorhydria. At least two distinct mechanisms of endogenous formation have been identified. The first, a direct chemical reaction between secondary amino compounds and nitrite, is strongly pH dependent and does not proceed rapidly at neutral pH even in the presence of chemical catalysts. The second depends on the direct bacterial catalysis of N-nitrosation. The data presented demonstrate that the bacterially mediated reaction is catalysed by bacterial enzyme systems and proceeds much more rapidly at neutral pH than the chemical reaction. This suggests a particular relevance to the in vivo situation where neutral pH, bacteria and elevated nitrite concentrations are found. Drawing on the kinetic information presented regarding the bacterially mediated nitrosation reaction, the known kinetics of the chemical reaction and the published values for the relevant substrate concentrations in both the colonised and the normal acid stomach the bacterial and chemical reactions have been compared. Using these criteria, and assuming the presence of bacteria with the appropriate metabolic activity, it may be predicted that N-nitroso compounds may be formed in the colonized stomach at much higher concentrations than in the normal acid stomach. The difference in yield may be by two to four orders of magnitude. Different bacterial species and different isolates of the same species show considerable variation in their abilities to catalyse N-nitrosation reactions. The most rapid catalysis is associated with those bacteria capable of reducing nitrate and nitrite by the process of denitrification. The most significant clinical corollary of these studies is that although bacterial catalysis of N-nitrosation has been demonstrated unequivocally, bacterial colonization of the stomach may not itself necessarily result in elevated endogenous N-nitroso compound exposure despite the elevated nitrite concentrations normally associated with such colonization. An increase in exposure to endogenously formed N-nitroso compounds would only be predicted in those individuals where a significant proportion of the colonizing bacteria expressed significant N-nitrosation activity. As a consequence the carcinogenic risk may be restricted to only a small proportion of colonized individuals depending on the prevalence of sustained infection by bacteria with significant N-nitrosation activity, particularly denitrifiers.

Humans↗
PubMed1994

Dietary factors and the risk of glioma in adults: results of a case-control study in Melbourne, Australia.

In a population-based case-control study of 416 incident gliomas in adults carried out in Melbourne, Australia, between 1987 and 1991, 409 age-sex-matched case-control pairs (243 male and 166 female) had adequate data available to examine associations between the dietary intake of N-nitroso compounds, N-nitroso precursors, other nutrients including N-nitroso inhibitors, and the risk of glioma. Dietary intakes were based on the reported frequency of consumption of 59 food items. Increased odds ratio (OR) were observed in males who consumed high levels of bacon, corned meats, apples, melons and oil. OR less than unity were observed in men consuming cabbage and cola drinks, and in women who consumed wholegrain bread, pasta, corned meat, bananas, cauliflower, brocoli, cola drinks and nuts. Generally, N-nitroso associations were greater in men and micronutrient associations were greater in women. Elevated OR in men, but not women, were associated with the intake of N-nitroso dimethylamine (NDMA), retinol and vitamin E. The intake of nitrate (largely of vegetable origin) was protective in women but not in men. When analyzed using multiple logistic regression, the association with NDMA intake in males was not modified by dietary micronutrient intakes. In females, beta carotene alone, though not directly associated with risk, modified the effect of NDMA. On balance, this study added only limited support to the N-nitroso hypothesis of glial carcinogenesis.

Australia↗
PubMed1999

Gas chromatographic-mass spectrometric detection of S-nitroso-cysteine and S-nitroso-glutathione.

A gas chromatographic-mass spectrometric (GC-MS) method is described for the quantitative determination of the S-nitroso compounds S-nitroso-cysteine (SNC) and S-nitroso-glutathione (GSNO) using their (15)N-labeled analogs, i.e., S(15)NC and GS(15)NO, as internal standards. The method is based on the specific conversion by HgCl(2) of the unlabeled and (15)N-labeled S-nitroso groups to nitrite and (15)N-nitrite, respectively, and their conversion to the pentafluorobenzyl derivatives. The method was applied to quantify GS(15)NO formed in the cytosol of washed human erythrocytes incubated with S(15)NC. Combination of high-performance liquid chromatography with GC-MS allowed specific and accurate quantification of SNC and GSNO externally added to human plasma ultrafiltrate (range 0-10 microM). Method accuracy and precision for SNC and GSNO were close to 100 and below 9%, respectively. As little as 0.1 nM GS(15)NO corresponding to 30 amol of (15)N-nitrite injected onto the column was precisely detected by the method.

Cysteine↗
PubMed2000

Inhibition of papain by S-nitrosothiols. Formation of mixed disulfides.

S-Nitrosylation of protein thiols is one of the cellular regulatory mechanisms induced by NO. The cysteine protease papain has a critical thiol residue (Cys(25)). It has been demonstrated that NO or NO donors such as sodium nitroprusside and N-nitrosoaniline derivatives can reversibly inhibit this enzyme by S-NO bond formation in its active site. In this study, a different regulated mechanism of inactivation was reported using S-nitrosothiols as the NO donor. Five S-nitroso compounds, S-nitroso-N-acetyl-dl-penicillamine, S-nitrosoglutathione, S-nitrosocaptopril, glucose-S-nitroso-N-acetyl-dl-penicillamine-2, and the S-nitroso tripeptide acetyl-Phe-Gly-S-nitrosopenicillamine, exhibited different inhibitory activities toward the enzyme in a time- and concentration-dependent manner with second-order rate constants (k(i)/K(I)) ranging from 8.9 to 17.2 m(-1) s(-1). The inhibition of papain by S-nitrosothiol was rapidly reversed by dithiothreitol, but not by ascorbate, which could reverse the inhibition of papain by NOBF(4). Incubation of the enzyme with a fluorescent S-nitroso probe (S-nitroso-5-dimethylaminonaphthalene-1-sulfonyl) resulted in the appearance of fluorescence of the protein, indicating the formation of a thiol adduct. Moreover, S-transnitrosylation in the incubation of S-nitroso inactivators with papain was excluded. These results suggest that inactivation of papain by S-nitrosothiols is due to a direct attack of the highly reactive thiolate (Cys(25)) in the enzyme active site on the sulfur of S-nitrosothiols to form a mixed disulfide between the inactivator and papain.

Binding Sites↗
PubMed1980

[Intragastral nitrosation - cancer risk in the operated stomach (author's transl)].

The concentration of nitrite and N-nitroso compounds was examined in the fasting gastric juice of 44 patients with regard to the known cancer risk to the operated stomach. All patients had surgery for therapy of an ulcer disease. The operation had taken place an average of 2.5 years previously. Enlisted as a control group were 26 age-matched individuals with healthy stomachs. The concentration of nitrite and N-nitroso compounds in the gastric juice of the vagotomized patiens (PGV) did not differ from that of the controls. On the other hand, a significant increase of the nitrite concentration was found in the gastric juice of those patients resected according to the Billroth I or II procedures. The fraction of N-nitroso compounds, however, was significantly elevated in relation to the other gastric juice samples only in the Billroth II resected stomach. The importance of the increase of nitrite and N-nitroso compounds to the cancer risk inherent in the gastric stump is the subject of discussion.

Gastrectomy↗