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PubMed1985

An example of interaction between environmental pollutants: modification of thiram toxicity to freshwater organisms by nitrites or nitrates in relation to nitrosamine synthesis.

Thiram, a dithiocarbamate fungicide, is known to evolve to dimethylnitrosamine (DMNA) when associated with nitrites. Conditions of appearance of that carcinogenic compound have been studied in short-term experiments by association of the fungicide, nitrates or nitrites, and species representative of freshwater biota. DMNA has been estimated by GLC equipped with a specific detector. Chlorella vulgaris can rapidly produce nitrites from nitrates and DMNA is obtained in presence of thiram. Daphnia magna can also synthesize DMNA but nitrites have to be added to the medium. Increased toxicity of thiram is observed. The same results are obtained on Cyprinus carpio and for a part on Brachydanio rerio. When the species are associated in a 15-day experimental food chain, and intoxicated algae feed the two other levels, no significant transfer is observed. Nevertheless, some DMNA hazard may exist for particular species exposed to thiram associated with nitrites or even nitrates if algae are present.

Animals↗
PubMed1976

Suppression of dimethylnitrosamine mutagenicity by nitrososarcosine and other nitrosamines.

Nitrososarcosine, not mutagenic itself in the host-mediated assay using Salmonella typhimurium G46 as indicator organism, lowered the mutant frequency produced by dimethylnitrosamine (DMN). Mutant frequency was significantly depressed when 1.0 g/kg nitrososarcosine was administered by gavage 0.5--2.0 h prior to intramuscular injection of 500 mg/kg DMN. Doses of nitrososarcosine as low as 37.2 mg/kg administered 45 min prior to dimethylnitrosamine treatment produced statistically significant reduction of mutant frequency. Dimethylnitrosamine, diethylnitrosamine and dibutylnitrosamine (500 mg/kg) also partially suppressed the mutant frequency produced by 500 mg/kg DMN when administered 45 min prior to dmn. diethylnitrosamine and dibutylnitrosamine were not found to be mutagenic in this test system.

Animals↗
PubMed1989

Transplacental genotoxicity of a tobacco-specific N-nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, in Syrian golden hamster.

NNK is abundant in cigarette smoke and is a potent respiratory carcinogen in adult Syrian golden hamsters. Micronucleus (MN) induction in fetal liver and maternal bone marrow polychromatic erythrocytes (PCEs) were assayed after i.p. injection of NNK to 14-day pregnant hamsters. The frequency of MN induction observed in fetal PCEs reached a maximum 18 h after treatment. The relationship dose NNK (0-200 mg/kg) to MN frequency was significant (P less than 0.005). In contrast no significant MN induction was observed in adult bone-marrow PCEs (P greater than 0.1). Extraction of fetal liver and amniotic fluid and HPLC separation of NNK metabolites revealed that NNK and its metabolite NNA1 could cross the placental barrier and be activated to protein-binding intermediates. These results suggest that NNK could be a transplancental carcinogen in Syrian golden hamsters.

Animals↗
PubMed1984

Detection of N-nitrosamines in the saliva of habitual chewers of tobacco.

The saliva of habitual chewers of tobacco and of non- chewers was examined using high-performance liquid chromatography and gas-liquid chromatography-thermal energy analysis. N-Nitrosodimethylamine, N-nitrosodiethylamine, N-nitrosopyrrolidine, N-nitrosonornicotine and N- nitrosohydroxyproline were detected in the saliva from the tobacco chewers . These N-nitroso compounds are probably leached from the tobacco itself and/or are formed in situ by the nitrosation of tobacco alkaloids as well as that of secondary amines. No N-nitroso compounds were detected in the saliva of non- chewers .

Adult↗
PubMed1987

Tobacco-specific N-nitrosamines in dry snuff.

Case-control studies have shown that the oral use of dry snuff has an aetiological association with cancer of the oral cavity. This communication reports high concentrations of the powerful carcinogen N'-nitrosonornicotine (9.37-55.3 micrograms/g), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (1.98-14.4 micrograms/g) and of N'-nitrosoanatabine (18.8-40.2 micrograms/g) and N'-nitrosoanabasine (0.66-1.17 microgram/g) in three popular brands of dry snuff available in the USA.

Alkaloids↗
PubMed1989

Influence of dietary protein and gut microflora on endogenous synthesis of nitrate and N-nitrosamines in the rat.

Groups of four germ-free (GF) and conventional (CV) rats were given purified diets containing either 50 or 200 g lactalbumin/kg for 2 wk and their urinary excretion of nitrate was measured. Urinary excretion of N-nitrosoproline was also measured in one of the three experiments. Both GF and CV rats given the high-protein diet excreted significantly more nitrate and N-nitrosoproline than those given the low-protein diet. On both diets GF rats excreted more nitrate than their CV counterparts but N-nitrosoproline excretion was not affected by environment. Groups of 11 GF and CV rats given diets containing sesame meal with or without a supplement of lysine-HCl for 2 wk, excreted similar amounts of nitrate on both diets, but more nitrate was excreted by GF rats than by their CV counterparts. N-nitrosoproline excretion by rats given the lysine supplement was higher in both environments. It is concluded that endogenous synthesis of nitrate is mediated by mammalian tissues rather than microflora and that dietary protein is an important source of nitrogen for the synthesis, although surplus amino acids from an imbalanced protein source do not act as precursors of endogenously formed nitrate. Some of the synthesized nitrate or its precursors appears to be metabolized by the microflora in the CV rat.

Animals↗
PubMed1980

Induction of local epidermal papillomas and carcinoma by selected nitrosamines.

Weekly cutaneous application of N-nitrosobis (2-oxopropyl)amine (BOP) at a dose of 2 mg/application to the neck area resulted in the induction of local papillomas and carcinomas in 80% of Syrian hamsters as early as 19 weeks post-treatment. In addition, a few tumors of internal organs (predominantly in the liver) were also found. N-Nitroso(2-hydroxypropyl) (2-oxopropyl)amine (HPOP), a common metabolite of BOP and BHP, was also found to be an epidermal carcinogen at a dose of 3.8 mg/application. N-Nitrosobis(2-hydroxypropyl)amine (BHP), however, failed to induce any epidermal lesions, when applied similarly at a much higher dose level (%) mg/animal/week). In contrast to BOP and HPOP, BHP induced a high incidence of tumors in internal organs, especially pancreatic cancer, which was the only induced tumor in 5 animals. Skin absorption studies demonstrated that BHP, but not BOP is rapidly absorbed and was detectable in the blood in concentrations of up to 5.5 mug/ml as early as 15 min after carcinogen administration. The possible reasons for the differing effects of BHP and BOP upon hamster skin are discussed.

Adenocarcinoma↗
PubMed1983

Effect of ethanol on early stages in nitrosamine carcinogenesis in rat liver.

The effect of chronic alcohol consumption on the extent of adenosine triphosphatase(ATPase)-deficient preneoplastic lesions in rat liver induced by either diethylnitrosamine (DEN) (3 mg/kg, p.o.) or N-nitrosomorpholine (NNM) (40 ppm in the drinking water) was studied. Carcinogens were administered on 4 days in every week for 11 (DEN) and 15 (NNM) weeks, respectively. Ethanol was given at a concentration of 10% (w/v) in the drinking water either during carcinogen treatment or after withdrawal of carcinogen. An increase in both number and size of ATPase-deficient foci in liver was observed when the alcohol was given during the period of carcinogen administration. This increase may be associated with the known toxic action of ethanol which leads to single cell necrosis and liver regeneration. In contrast, when ethanol (10% in the drinking water for 16 weeks) was given after cessation of carcinogen treatment following a tumor-promotion feeding protocol, no such enhancement in preneoplastic response was obtained. Ethanol alone was ineffective in inducing ATPase-deficient foci. In liver, ethanol thus appears to possess, under certain conditions, co-carcinogenic but not tumor-promoting capacity.

Adenosine Triphosphatases↗
PubMed1983

Spongiosis hepatis in rats treated with low doses of hepatotropic nitrosamines.

Spongiosis hepatis, a characteristic pathomorphologic entity originating from the perisinusoidal liver cells, was observed in rats after administration of relatively low doses of the hepatocarcinogens dimethylnitrosamine (DMNA) and nitrosopyrrolidine (NO-Pyr), but not after application of the urinary bladder carcinogen butyl-butanolnitrosamine (BBNA). The results support the conception that spongiosis is a persisting liver lesion due to specific changes of the perisinusoidal liver cells by hepatotropic carcinogens.

Animals↗
PubMed1986

Formation of an N-nitrosamine by oxidation.

Tolazamide, an antidiabetic drug, was found to produce N-nitrosohexamethyleneimine (NHM) upon exposure to an oxidizing agent and in the absence of a nitrosating agent. The oxidizing agents were either hydrogen peroxide or oxygen.

Carcinogens↗
PubMed1987

Micronucleus formation induced in rat liver and esophagus by nitrosamines.

The rat hepatocarcinogen nitrosodimethylamine and the esophageal carcinogens nitrosomethylbenzylamine and nitrosomethylamylamine were shown to produce chromosomal damage, as manifested by micronucleus formation, in their target tissues. There was cross-reactivity in the two tissues, however, at high dose levels. Nitrosodiethylamine, which produces tumors in both the liver and esophagus in the rat, also produced micronuclei in both tissues.

Animals↗
PubMed1988

Differential induction of DNA strand breaks by nitrosamines in the rat liver and esophagus.

Hepatic and esophageal nuclei were isolated from Sprague-Dawley rats treated with 5 mg/kg dimethylnitrosamine (DMN), 100 mg/kg diethylnitrosamine (DEN) and 2.5 mg and 10 mg/kg methylbenzylnitrosamine (MBN) and subjected to alkaline elution to determine DNA strand breaks and their subsequent repair. Results obtained showed that hepatic nuclei isolated from rats 4 h after treatment by either DMN or DEN had about 60% of the DNA eluting through the filter. However, at 12 h post treatment, while about 50% of the single-strand breaks in dimethylnitrosamine treated rats were repaired, only about 10-15% of such breaks induced by DEN were repaired in the liver. That DEN is a more effective inducer of hepatic preneoplastic lesions could thus be attributed to this slow repair of the DEN induced lesions. Strand breaks were neither induced by DMN in the esophagus nor by MBN in the liver, the nontarget tissues. More surprising, however, was the finding that MBN induced little or no single-strand breaks in its target tissue, the esophagus. Furthermore, there was no evidence for DNA-protein cross-linking or alkali labile sites in the esophageal DNA. The results indicate that DNA damage induced by the initiating carcinogen in the target tissue may not necessarily involve strand breaks.

Animals↗