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PubMed1993

Induction of chromosomal aberrations, sister-chromatid exchanges and cell-cycle delay in cow peripheral blood lymphocytes treatment with two N-nitroso compounds in vitro.

We investigated the effect of NDMA and DNSGU on the induction of chromosomal aberrations and sister-chromatid exchanges (SCEs), as well as the influence of the former compound on cell-cycle kinetics in cultured cow peripheral lymphocytes. A clastogenic effect was observed in treated cell cultures at 6 or 12 x 10(-5) M concentrations of NMDA and DNSGU, respectively, but no increase of chromosomal breaks was seen at the lowest dose. NDMA at 6 x 10(-4) M was toxic to cow lymphocytes. NDMA and DNSGU induced statistical increases of SCEs at the test doses (6 or 12 x 10(-6) and 6 or 12 x 10(-5) M, respectively). In addition, treatment with NMDA at a dose of 6 x 10(-5) M revealed significant heterogeneity of the first, second and third metaphases between treated and untreated groups. A reduction of the proliferation index and proliferation delay per cycle was shown too.

Analysis of Variance↗
PubMed1976

Carcinogenic effects of different nitroso-compounds in chinese hamsters: N-dibutylnitrosamine and N-nitrosomethylurea.

Three hundred and twenty Chinese hamsters (Cricetulus griseus) (CH) were subcutaneously (s.c.) treated with 1/5, 1/10 or 1/20 the mean lethal dose (LD50) of N-dibutylnitrosamine (DBN) or N-nitrosomethylurea (NMU). In several respects these two substances produced the same organotropy in the CH as in the Syrian golden (SGH) and European hamsters (EH). DBN prolonged lung tumours and neoplasms of the injection site. NMU induced tumours of the injection site only.

Animals↗
PubMed2003

Detection of in vivo genotoxicity of endogenously formed N-nitroso compounds and suppression by ascorbic acid, teas and fruit juices.

The genotoxicity of endogenously formed N-nitrosamines from secondary amines and sodium nitrite (NaNO(2)) was evaluated in multiple organs of mice, using comet assay. Groups of four male mice were orally given dimethylamine, proline, and morpholine simultaneously with NaNO(2). The stomach, colon, liver, kidney, urinary bladder, lung, brain, and bone marrow were sampled 3 and 24 h after these compounds had been ingested. Although secondary amines and the NaNO(2) tested did not yield DNA damage in any of the organs tested, DNA damage was observed mainly in the liver following simultaneous oral ingestion of these compounds. The administration within a 60 min interval also yielded hepatic DNA damage. It is considered that DNA damage induced in mouse organs with the coexistence of amines and nitrite in the acidic stomach is due to endogenously formed nitrosamines. Ascorbic acid reduced the liver DNA damage induced by morpholine and NaNO(2). Reductions in hepatic genotoxicity of endogenously formed N-nitrosomorpholine by tea polyphenols, such as catechins and theaflavins, and fresh apple, grape, and orange juices were more effective than was by ascorbic acid. In contrast with the antimutagenicity of ascorbic acid in the liver, ascorbic acid yielded stomach DNA damage in the presence of NaNO(2) (in the presence and absence of morpholine). Even if ascorbic acid acts as an antimutagen in the liver, nitric oxide (NO) formed from the reduction of NaNO(2) by ascorbic acid damaged stomach DNA.

Animals↗
PubMed1993

A redox-based mechanism for the neuroprotective and neurodestructive effects of nitric oxide and related nitroso-compounds.

Congeners of nitrogen monoxide (NO) are neuroprotective and neurodestructive. To address this apparent paradox, we considered the effects on neurons of compounds characterized by alternative redox states of NO: nitric oxide (NO.) and nitrosonium ion (NO+). Nitric oxide, generated from NO. donors or synthesized endogenously after NMDA (N-methyl-D-aspartate) receptor activation, can lead to neurotoxicity. Here, we report that NO.- mediated neurotoxicity is engendered, at least in part, by reaction with superoxide anion (O2.-), apparently leading to formation of peroxynitrite (ONOO-), and not by NO. alone. In contrast, the neuroprotective effects of NO result from downregulation of NMDA-receptor activity by reaction with thiol group(s) of the receptor's redox modulatory site. This reaction is not mediated by NO. itself, but occurs under conditions supporting S-nitrosylation of NMDA receptor thiol (reaction or transfer of NO+). Moreover, the redox versatility of NO allows for its interconversion from neuroprotective to neurotoxic species by a change in the ambient redox milieu. The details of this complex redox chemistry of NO may provide a mechanism for harnessing neuroprotective effects and avoiding neurotoxicity in the central nervous system.

Animals↗
PubMed1976

Carcinogenic effects of different nitroso-compounds in Chinese hamsters. I. Dimethylnitrosamine and N-diethylnitrosamine.

Three hundred and twenty Chinese hamsters (Cricetulus griseus) (CH) were treated (s.c.) with 1/5, 1/10 or 1/20 LD50 of dimethylnitrosamine (DMN) or N-diethylnitrosamine (DEN). These substances, in several respects, showed a different organotropy in this species than in both the Syrian golden (SGH) and the European hamster (EH). In CH, DEN produced up to 100% squamous cell papillomata and occasionally also carcinomata of the cheek pouch, tongue, pharynix, oesophagus and forestomach. With DEN a high rate of hepatomata was simultaneously realized. DMN induced a considerable quantity of liver tumours, the highest incidence being demonstrated in the lowest dosage group.

Animals↗
PubMed1999

Evidence for involvement of nitric oxide (NO) or a related nitroso-compound in NANC inhibitory neurotransmission in the pigeon oesophageal smooth muscle.

In the pigeon oesophageal smooth muscle electrical field stimulation (EFS), in the presence of atropine and guanethidine, evoked TTX-sensitive inhibitory effects on both the electrical and mechanical activity. N(omega)-Nitro L-arginine (L-NA) (0.1-100 microM), an inhibitor of nitric oxide synthase, reduced the inhibitory EFS-evoked effects. Sodium nitroprusside (SNP) (10 microM), a NO-donor, mimicked the effects evoked by EFS. Apamin (1 microM) perfusion did not modify the inhibitory effects induced by SNP. Cystamine (10 microM), a guanylate-cyclase inhibitor, reduced the inhibitory effects elicited by EFS. This study shows a possible role for NO in the non-adrenergic non-cholinergic (NANC) inhibitory responses induced by EFS in the pigeon oesophagus.

Adrenergic Agents↗
PubMed1986

N-nitroso-hydroxyalkyl-alkylamine phosphate esters--a new class of N-nitroso compounds.

A new class of phosphate-esterified alpha-hydroxyalkyl-alkyl-nitrosamines is described. Here we report the synthesis of these compounds. The mechanism of their formation from the corresponding alpha-acetoxy compounds, and starting from alpha-hydroperoxy compounds is studied by monitoring the reactions in the u.v.-spectrophotometer, by reaction with alkaline phosphatase and by determination of aldehydes generated during degradation of the N-nitrosoacetylesters. Their stability in aqueous solution and their phosphatase-induced degradation was determined. It was found that alpha-phosphate-nitrosamines are more stable in aqueous solution than the alpha-acetates or the parent alpha-hydroxy compounds. Therefore their role as intermediates in nitrosamine metabolism is discussed.

Alkaline Phosphatase↗
PubMed1982

Studies on the enzymatic reduction of C-nitroso compounds. V. Molecular properties of porcine heart C-nitrosoreductase and identity of this enzyme with NAD(P)H dehydrogenase.

NAD(P)H-dependent C-nitrosoreductase of porcine heart cytosol was purified 12,000-fold in the presence of NADH with an overall yield of 2.2%. The purification procedure included ammonium sulfate fractionation, gel filtration with Sephadex G-100, ion-exchange chromatography on DEAE-Sephadex A-50, hydrophobic chromatography on Octyl-Sepharose CL-4B, and gel filtration with Sephadex G-200. The purity of the preparation was approximately 90% and the molecular weight of the enzyme estimated by gel filtration was about 60,000. The purified enzyme was composed of two molecular forms, nitrosoreductases 1 and 2, having isoelectric points of 8.45 and 8.6, respectively. A significant amount of zinc was found in the preparation by X-ray fluorescence analysis. The enzyme as it was prepared was colorless, but, after oxidation with p-nitrosophenol followed by gel filtration in the absence of NADH, it showed the absorption spectrum of a flavoprotein. Spectral data indicated the presence of 1 mol of flavin per mol of the enzyme. The molecular turnover number was calculated to be 10,000 nmol p-nitrosophenol reduced to p-aminophenol per min per nmol enzyme at pH 5.8 and 22 degrees C. The activity was inhibited by p-chloromercuribenzoate by 50% at a concentration of 3 x 10(-5) M. Besides the nitrosoreductase activity, the purified preparation showed NAD(P)H-dependent menadione reductase activity. The activities were both strongly inhibited by dicumarol and markedly activated by serum albumin and by Tween 20. These results indicate the probable identity of this enzyme with soluble NAD(P)H dehydrogenase (quinone) [EC 1.6.99.2].

Alcohol Oxidoreductases↗
PubMed1980

N-nitroso compound precursors and gastric cancer: preliminary data of a study on a group of farm workers.

An epidemiological research on gstric cancer mortality rates carried out in the town of Forì is reported. The results are significant as regards the relation between the urban and rural areas, and show a higher risk for gastric cancer in the rural area. Salivary nitrite measurement in 92 farm workers showed particularly high values (over 30 ppm in 4 individuals). Analysis of histological findings in biopsies performed during endoscopy in 46 persons of the group studied showed a great number of CAG and CAG + IM in asymptomatic individuals.

Adult↗