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PubMed1980

Studies on the enzymatic reduction of C-nitroso compounds. III. The kinetic analysis of C-nitrosoreductase reaction catalyzed by the cytoplasmic enzyme from porcine liver.

The reaction kinetics of the major cytoplasmic NADH-nitrosoreductase, which is the identical enzyme to alcohol dehydrogenase [EC 1.1.1.1], was studied with a partially purified preparation from porcine liver. On the basis of the data obtained, the following scheme is proposed as the mechanism of this enzyme reaction: [Formula: see text], where E and E' are the enzyme unit (one subunit of alcohol dehydrogenase) and an intermediate form of the enzyme unit-substrate compound which appears by two-electron reduction of the enzyme unit-substrate compound, respectively, S is p-nitrosophenol (p-NSP), N is NADH, and P1 and P2 are NAD+ and p-aminophenol (p-AmP), respectively. In this case, it is assumed that k1 less than K2. Para-aminophenol, the reaction product, showed an inhibition competitive to p-NSP at fixed concentrations of NADH and also showed a mixed-type inhibition to NADH at fixed concentrations of p-NSP. NAD+ inhibited the reaction in a competitive manner to NADH at fixed concentrations of p-NSP and in a non-competitive manner to p-NSP at fixed concentrations of NADH. These results can also be accounted for by the proposed mechanism.

Alcohol Oxidoreductases↗
PubMed1989

[The role of UDP glucuronosyl- and sulfotransferases in the butylhydroxytoluene suppression of the mutagenic action of carcinogenic nitroso compounds and cyclophosphane].

Treatment with butylated hydroxytoluene (BHT) was shown to stimulate the activity of UDP-glucuronosyltransferase and to inhibit that of sulfotransferase in liver of Wistar male rats. Addition of UDP-glucuronic acid to incubation medium in Ames' test using BHT-pretreated subfractions of rat liver resulted in decreased mutagenicity of nitrosodiethylamine, nitrosomorpholine and cyclophosphamide. Further treatment with 3'-phosphoadenosine-5'-phosphosulfate failed to affect mutagenic activity of the promutagens tested. However, an increase in mutagenicity of nitrosomorpholine and cyclophosphamide was observed in application of liver subfractions from intact animals. It was concluded that BHT-induced inhibition of active metabolite production as well as increased production of their glucuronides are responsible for inhibition of mutagenicity of the agents tested. Simultaneous decrease in the yield of sulfates potentiated this effect for nitrosomorpholine and cyclophosphamide.

Animals↗
PubMed1989

[Characteristics of action of precursors of carcinogenic nitroso-compounds on cell cultures].

On the primary rat lung cell cultures, a study was made of the transforming action of sodium nitrite (NN) and amidopyrine combination with the control for formation of carcinogen--N-nitrosodimethylamine (NDMA) in growth medium. The manifestation of transformation was registered by appearance of morphological changes and multilayer growth foci. As criteria for evaluation after 48 hour treatments with NDMA, NN and AP, were used DNA-synthetizing activity of cells, mitotic index, frequency of mitoses pathology, monolayer density. The effects of transforming dose of NN alone and in combination with AP were the same. But malignization (tumor development in newborn rats in the points of cell suspension inoculation) took place only after administration of NN in combination with AP, when carcinogen was formed. Theophylline decreased the action of NN-AP combination.

Aminopyrine↗
PubMed1988

Urinary N-nitrosamino acids as an index of exposure to N-nitroso compounds.

On the basis of results from animal experiments and studies in human subjects, the amount of nitrosoproline (NPRO) excreted in 24-hr urine following ingestion of precursors (proline, nitrate) has been measured as an index of endogenous nitrosation. Several protocols of the NPRO test have been applied to human subjects, in order to study the kinetics and dietary modifiers of endogenous nitrosation, and in clinical and epidemiological studies. These studies have demonstrated that endogenous nitrosation in humans is highly complex and is influenced by factors such as gastric pH and amounts of precursors, catalysts and inhibitors. Thus, individual monitoring for nitrosation potential, rather than analyses of precursors in saliva, urine and gastric juice, is necessary in order to establish a causal relationship between endogenous nitrosation and human cancer. Results obtained after application of the NPRO test to subjects at high risk for cancers of the stomach, oesophagus, oral cavity and urinary bladder are summarized.

Environmental Monitoring↗
PubMed1980

Occurrence, formation and precursors of N-nitroso compounds in the Japanese diet.

A survey has been made of volatile nitrosamines in 123 fermented foods. These included salt-fermented vegetables, soy sauce, "miso", Japanese "sake" and other fermentation products. No appreciable amount, or only trace quantities, of NDMA and NPYR were detected in vinegar, "sake", wines and whiskies, while minute quantities of NDMA were detected in 31 out of 33 beer samples, where the levels ranged from traces to 13.8 micrograms/l, with an average of 5.1 micrograms/l. The nitrosamine content of salt-dried fish apparently increased when these products were broiled in a city gas range. A method for the determination of N-alkylureas in foods has been developed. A total of 57 food samples, both uncooked and broiled in a gas range or fried, were analysed. No alkylureas could be detected in these samples.

Animals↗
PubMed1997

Effect of nitroso compounds on Na/K-ATPase.

Thiol containing NO.-derivatives were found to inhibit the activity of brain and kidney Na/K-ATPase. S-Nitrosogluthatione demonstrated only minor inhibiting activity, while dinitrosyl iron complexes (DNIC) with cysteine or glutathione were much more effective. Brain Na/K-ATPase is more vulnerable to inhibiting action than kidney Na/K-ATPase. Inhibition of the activity is accompanied by a decrease in amount of protein thiol groups and a change in the substrate dependence curve of the enzyme. Restoration of Na/K-ATPase activity by SH-reagent dithiothreitol or cysteine is accompanied by restoration of SH-groups of the enzyme. This suggests that blockade of SH-groups of Na/K-ATPase is responsible for the inhibition. The possibility that this blockade results in disordering of interprotomer interactions within the oligomeric complexes of Na/K-ATPase is suggested. Possible regulatory meaning of the effect of NO. derivatives is discussed.

Animals↗
PubMed1987

[Butylhydroxytoluene inhibition of the mutagenic activity of carcinogenic nitroso compounds and cyclophosphamide: the role of the glutathione conjugation reaction].

Mutagenic effect of diethylnitrosamine, nitrosomorpholine and cyclophosphamide were studied on Salmonella typhimurium in the Ames test using S9, microsomal and cytosolic subfractions of Wistar male rats. Pretreatment with butylhydroxytoluene (BHT) was followed by a 50-60% decrease in metabolic activation of the said promutagens by liver subfractions. This was matched by an increase in cytosolic and microsomal glutathione-S-transferase activity and glutathione level in rat liver. The addition of glutathione to the incubation medium in the Ames test using liver subfractions of BHT-treated rats brought on a complete inhibition of mutagenic effect of the agents studied. It is suggested that BHT-induced decrease in production of active metabolites and increase in their inactivation in reactions of glutathione enzymatic conjugation account for the inhibition of mutagenicity of the promutagens under study.

Animals↗
PubMed1994

Experimental evidence for inhibition of N-nitroso compound formation as a factor in the negative correlation between vitamin C consumption and the incidence of certain cancers.

Ascorbic acid (ASC) consumption is negatively correlated with the incidence of certain cancers. This is a review and update of the theory, which has recently been neglected, that this negative correlation is due to ASC inhibition of in vivo nitrosation. The review covers the older literature on ASC inhibition of carcinogenesis by nitrite administered with amines or amides and more recent studies on ASC inhibition of nitrosation by bacteria, nitrogen oxides, and activated macrophages; the role of oxygen in ASC inhibition of gastric nitrosation; ASC inhibition of N-nitrosoproline formation in subjects from areas with high incidences of certain cancers; dose and temporal relationships between ASC and in vivo nitrosation in humans; the role of substances other than ASC in the inhibition of nitrosation by vegetables and fruits; and the active secretion of ASC into the human stomach.

Animals↗
PubMed1983

Use of pancreatic beta cells in culture to identify diabetogenic N-nitroso compounds.

Epidemiological observations suggest that environmental factors play a role in the pathogenesis of insulin dependent diabetes mellitus (1). Several chemicals have been identified as specific beta cell toxins (2-4). We report here studies to determine the feasibility of using monolayer cultures of pancreatic beta cells from neonatal rat to screen potential diabetogenic chemicals. Cytotoxicity was monitored both by phase microscopy and the release of insulin into the culture medium. In comparative studies, cellular protein and release of 51chromium (51Cr) were measured after addition of test compounds to cultures of fibroblasts derived from pancreatic tissue. The nitrosoamides 1 methyl-l-nitrosourea (MNU), 1,3 bis (2-choroethyl) nitrosourea (BCNU), chlorozotocin (CLZ), and the beta cell toxin, streptozotocin (SZ), were examined. CLZ and SZ were more toxic to pancreatic beta cells than to fibroblasts. In contrast, MNU and BCNU damaged both beta cells and fibroblasts at identical concentrations. These results suggest that in vitro techniques can be used to identify chemicals that selectively injure beta cells. Although SZ-induced toxicity was ameliorated with addition of nicotinamide to cultures of beta cells, nicotinamide did not prevent damage caused by CLZ. This observation indicates different mechanisms of drug-induced cytotoxicity.

Animals↗
PubMed1979

The action of rat cytosol enzymes on some methylated nucleic acid components produced by the carcinogenic N-nitroso compounds.

The stabilities of several alkylated nucleic acid components have been examined in the presence of cytosol extracts from a variety of rat tissues. An activity capable of demethylating O6-methyldeoxyguanosine was readily detectable in all tissues examined; arranged in approximate order of decreasing specific activity these are as follows: small intestine, spleen, kidney, lung, liver, skin, heart and brain. The in vitro requirements for the activity derived from liver and the observations that O6-methylguanine and its deoxynucleoside 5'-monophosphate are insensitive to the action of these extracts suggests that this activity may be due to an enzyme which resembles adenosine deaminase. In contrast to the ready degradation of O6-methyldeoxyguanosine the corresponding ethyl derivative was degraded very much more slowly but there was no evidence for other activities against the O4- and O2-methyldeoxythymidines. Similarly, no demethylation of the N-substituted deoxynucleosides, 3-methyldeoxycytidine 3-methldeoxythymidine, 1-methyldeoxyadenosine and 7-methyldeoxyguanosine, was detected.

Animals↗
PubMed1989

Preformed N-nitroso compounds in foods and beverages.

Most western-style foods have been analysed for the presence of volatile N-nitrosamines. Relatively few foods consistently contain detectable (greater than 0.1 microgram/kg) amounts of volatile N-nitrosamines. The major known contributors to dietary volatile N-nitrosamines are nitrite-cured meats, particularly fried bacon, and beer. The amount of volatile N-nitrosamines in these foods has declined in recent years. Average dietary intakes of preformed volatile N-nitrosamines have been calculated from these data and indicate that dietary exposure for consumers of western-style foods amounts to 0.5 to 1.0 microgram/day/person. Asian foods have not been surveyed to the same extent but preliminary data indicate a somewhat higher and more frequent volatile N-nitrosamine content, in part due to differences in fish intake and preparation. Indirect evidence suggests that the non-volatile content of some foods may be one to three orders of magnitude higher than volatile N-nitrosamine content.

Beverages↗
PubMed1994

Biological studies of a nitroso compound that releases nitric oxide upon illumination.

2-Methyl-2-nitrosopropane (MNP) has long been known to undergo photochemical and thermal decomposition, generating di-tert-butyl nitroxide, in organic solvent. The present study was undertaken to demonstrate that MNP can be used as a caged-nitric oxide (NO), which can liberate NO upon illumination. Photolysis of MNP leads to the generation of tert-butyl radical and NO, as detected by spin-trapping/ESR spectroscopy and by oxyhemoglobin/visible spectroscopy, respectively. Using soluble guanylate cyclase in neuroblastoma N1E-115 cells as an NO target, we found that MNP in the presence of light caused a dose- and time-dependent increase in cGMP. Finally, illumination of a solution of MNP was also found to induce relaxation of preconstricted isolated rat pulmonary artery rings. These studies demonstrated that MNP can be useful biochemical research tool for delivering NO in a controlled manner, by using light.

Animals↗
PubMed1986

Nitrate and nitrite in normal gastric juice. Precursors of the endogenous N-nitroso compound synthesis.

The nitrate and nitrite levels of 75 gastric juice samples from young and healthy fasting volunteers were examined. For both parameters a dependence on the specific pH value of the secretion was detected. The rise of the nitrite level from normal 0.1 ppm in the acid to 1.4 ppm in the neutral range can be explained by the activity of the bacterial flora even in the healthy stomach, which has already been demonstrated earlier. The hitherto existing theory that nitrate originates exclusively from the salivary glands, and if not reduced to nitrite by bacteria in the mouth cavity, is brought into the stomach via swallowed saliva only, does not explain the observation that there is a rise in nitrate concentration in neutral juice, too. Further investigations have to be made to see whether there are other endogenous sources of nitrate except the salivary glands in the gastrointestinal tract. The environmental pollutant nitrate must be paid more attention to in future.

Adult↗
PubMed2003

Measurement of nitric oxide in hippocampal slices: induction with nitroso compounds and the effect of depolarization.

Nitric oxide not only acts as a messenger for different physiological processes, but also mediates neurotoxicity associated with a variety of neurological disorders including epilepsy. The molecular mechanisms behind these actions are unclear. In this study, we aimed to detect relative amounts of NO released from rat hippocampal slices by chemiluminescence measurements under NMDA stimulation and spontaneous depolarization conditions. Hippocampal slices were preferred because of their functional integrity useful in simulating in vivo conditions. The reliability of the system was verified by administering increasing concentrations of a NO donor sodium nitroprusside in different redox milieu and a NO scavenger, carboxy-2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (carboxy PTIO). The redox versatility of NO allows interconversion from neuroprotective to neurotoxic species by a change in the ambient redox milieu. We have quantitated NO formed under NMDA stimulation and spontaneous depolarization conditions, and showed that depolarization increased NO formation and was excitotoxic for the neural tissue.

Acridines↗
PubMed1975

Dietary modifications affecting the mutagenicity of N-nitroso compounds in the host-mediated assay.

The effects of various dietary modifications on the mutagenicity of dimethylnitrosamine (DMNA), N-nitrosomorpholine, and N-methyl-N-nitrosourea for Salmonella typhimurium his G-46 in the host-mediated assay were studied. The diets used were:chow, complete semisynthetic, protein-free, and all-casein, in addition to a 24-hr starvation regimen. The mutagenicity of DMNA and N-nitrosomorpholine, which require metabolic activation for their biological activity, was depressed by the complete semisynthetic diet, as compared to the mutagenicity in mice fed the chow diet. DMNA mutagenicity was depressed by the protein-free diet and enhanced by pure casein as compared with the complete semisynthetic diet. N-Nitrosomorpholine mutagenicity was enhanced by starvation, but results with mice fed the protein-free and all-casein diets were ambiguous. N-Methyl-N-nitrosourea, which does not require metabolic activation for its biological activities, responded in an opposite manner to that of DMNA; its mutagenicity was enhanced by the complete semisynthetic and protein-free diets, but was depressed by the all-casein diet.

Animals↗
PubMed2005

Total antioxidant status in the blood serum of rats exposed to N-nitroso compounds and nitric oxide synthase inhibitors.

In this study, the total antioxidant status (TAS) was assayed in the blood serum of rats pretreated per os with either N-nitrosodiethylamine (NDEA) (0.1 mg/kg b.w./day) or N-methyl-N-nitrosourea (NMU) (0.1 mg/kg b.w./day) for 30 days. The animals were also dosed per os with spermidine (SPR) (10 mg/kg b.w./day) for a first 21 day period, and Nomega)-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg b.w./day) given to animals for 3 days (days 22-24), respectively. Nitric oxide synthase (NOS) inhibitor, L-NAME was found to mitigate TAS levels in the blood serum of rats pretreated with NDEA and NMU. No such changes were found in animals dosed with L-NAME only nor even with L-NAME and spermidine, respectively. Since spermidine, also known as an inhibitor of iNOS synthesis, elevated TAS levels in rats dosed with L-NAME and NDEA/NMU, the polyamine was suggested to modify the NOS/NO origin to serve the physiological level of the total anti-oxidant status in rat blood serum.

Animals↗
PubMed1987

A correlation study on urinary excretion of N-nitroso compounds and cancer mortality in China: interim results.

Samples of 12-h overnight urine were collected from approximately 40 male adults in each of the 26 counties of China. Two urine specimens were collected from each subject--one after a loading dose of proline and ascorbic acid and another after a loading dose of proline only. Levels of N-nitrosamino acids, nitrite and nitrate were measured in urine samples and correlated with cancer mortality per 100,000 male subjects in the truncated age range 35-64 years. Preliminary results show no clear correlation between presence of stomach cancer or liver cancer and nitrosation potential [as measured by the urinary level of N-nitrosoproline (NPRO) after the proline load test or of nitrate]. There was a moderate, although not clearly significant, tendency for oesophageal cancer mortality rates to be associated positively with nitrosation potential and negatively with background ascorbate levels in plasma. This result was due chiefly to the inclusion of one county (Song Xian) in which there is a fairly high oesophageal mortality rate, an average nitrosation potential three times greater than that of any other county, and the lowest ascorbate index of any county. Further study of this county is planned.

Adult↗
PubMed1975

Mutagenic selectivity of carcinogenic nitroso compounds 2. n-methyl-N-nitrosourethane.

The mutagenicity of the carcinogen methylnitrosourethane (MNUr) was examined in Drosophila with a view to the determination of its activity on heterochromatic loci (especially rDNA) relative to those in the euchromatin. Assays were made of the yield of rDNA mutations (bobbed: bb) relative to other X-chromosome recessive lethals and visibles [X(l + v)] in the same male germ cells after treatment with different doses (1-10 mM) and at various stages in spermatogenesis. Dose dependence followed the same pattern for all genic loci and germ cell stages. In all instances, the regression of mutation frequency on injected molar dose was approximately linear, but could better be described by a quadratic dose curve. In contrast, the mutagenicity pattern during spermatogenesis varied according to the target genes. The response of the euchromatic loci reached a peak among the earlier germ cells (probably the spermatocytes), whereas that for the heterochromatic sites (including rDNA) was maximal in mature sperm. Mutagenic selectivity for rDNA with MNUr, as indicated by the percentage bb/X-mutations, was among the highest for the intrinsically reactive carcinogens (alkylating and arylating agents). This correlates with the strong carcinogenicity of MNUr and adds further support to the concept that rDNA mutations might well be a crucial step in cancer initiation.

Animals↗