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Results for “NITROSAMINES”

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At least 1,495 records · Page 83Linked to original sources
PubMed1985

Sequential studies on the development of nitrosamine-induced pancreatic carcinoma in the Syrian golden hamster.

An attempt was made to define the importance of accumulated carcinogen dose and of induction-time on the development of pancreatic tumors after administration of N-nitrosobis(2-hydroxypropyl)amine (BHP) to Syrian golden hamsters. The development and progression of ductal hyperplasia, the number of tumor-bearing animals, the number of cancer-bearing animals, the number of tumors per tumor-bearing animal, and the grade of histological differentiation were found to be related to the accumulated dose of the carcinogen given, as was survival-time. The duration of the period between the carcinogen administration and examination was another factor of importance for the same changes except for the grade of histological differentiation of cancers and for survival-time. Once ductal hyperplasia and tumor development had started, there were no signs of regression - but rather progression - even after cessation of carcinogen administration. It is concluded that the development (progression) of induced pancreatic cancer in the Syrian golden hamster is influenced by the accumulated carcinogen (BHP) dose and the duration of the experiment. The results emphasize the need for a strict standardization of the experimental design as well as for the histological evaluation when animal models are used for studies of the effect of factors or procedures with a possible influence on the rate of tumor development.

Animals↗
PubMed1993

Intragastric nitrosation of nicotine is not a significant contributor to nitrosamine exposure.

To determine the potential for intragastric nicotine nitrosation, we carried out a kinetic study of the reaction of nicotine with nitrous acid in aqueous solution. The reaction of nicotine with nitrous acid resulted in the formation of three products, NNA, NNN, and NNK. The three parallel reactions were first order of 10-6 L/mol/s. The optimum pH range for formation of NNA, NNN, and NNK was 2.4 to 3.1. Thiocyanate (100 mM) slightly increased the rate of formation of NNN and NNK but tripled the rate of formation of NNA at pH 3.5 at 37 degrees C. We have also studied the nitrosation of pseudooxynicotine, a bacterial and fungal metabolite of nicotine. This secondary amine nitrosated rapidly to produce NNK. Our proposed mechanism for the conversion of nicotine to NNK includes nine kinetically distinct steps and is in agreement with our experimental results. The rate limiting step involves the formation of nicotine-1',2'-iminium ion. This ion hydrolyzes to form pseudooxynicotine which undergoes rapid, irreversible nitrosation to NNK. Given the very slow rate of nicotine nitrosation, it is unlikely that nicotine itself contributes to exposure to nitroso compounds due to chemically mediated intragastric nitrosation.

Butanones↗
PubMed1979

N-nitrosamines in the rubber and tire industry.

Airborne N-nitrosomorpholine (0 to 27 micrograms per cubic meter) was found in two of four rubber industry factories. N-Nitrosodimethylamine was also found in two factories, but at lower levels. These findings may be relevant to the reported increased risk of certain types of cancer in rubber workers in some of the same areas where the N-nitrosomorpholine levels were highest.

Air Pollutants↗
PubMed1973

Microbial formation of nitrosamines in vitro.

Mortierella parvispora and an unidentified bacterium converted trimethylamine to dimethylamine, and the bacterium (but not the fungus) formed dimethylnitrosamine in the presence of nitrite. Dimethylnitrosamine also appeared in cell suspensions of Escherichia coli and Streptococcus epidermidis and in hyphal mats of Aspergillus oryzae incubated with dimethylamine and nitrate. Suspensions of a number of microorganisms produced N-nitrosodiphenylamine from diphenylamine and nitrite at pH 7.5, and soluble enzymes catalyzing the N-nitrosation of diphenylamine were obtained from two of these organisms. In the presence of these enzymes, several dialkylamines were converted to the corresponding N-nitroso compounds.

Aspergillus↗
PubMed2005

Angiotensin II type 2 receptor gene deficiency attenuates susceptibility to tobacco-specific nitrosamine-induced lung tumorigenesis: involvement of transforming growth factor-beta-dependent cell growth attenuation.

To clarify an involvement of angiotensin II signaling in lung neoplasia, we have examined the effect of angiotensin II receptor deficiency on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis. Male angiotensin II type 2 receptor (AT2)-null mice with an SWR/J genetic background and control wild-type mice were treated with NNK (100 mg/kg, i.p.) or saline vehicle. NNK treatment caused the development of lung tumors in all wild-type control mice (100 % tumor prevalence), but only 85% of AT2-null mice developed tumors. The tumor multiplicity in AT2-null mice (1.9 +/- 0.3) was significantly smaller than that in wild-type mice (4.1 +/- 0.9). Primary cultured lung fibroblasts prepared from both AT2-null and wild-type mice markedly increased the colony counts of A549 lung cancer cells in soft agar, but a consistently higher colony count was observed with the wild-type fibroblasts (fold increase in colony number, 5.6 +/- 0.5) than with the AT2-null fibroblasts (3.5 +/- 0.8). The underlying mechanism by which angiotensin II regulates cancer cell growth is due to the regulation of active transforming growth factor-beta (TGF-beta) production. Although the total level of TGF-beta was significantly stimulated when A549 cells were cocultured with either type of fibroblasts, the level of active TGF-beta in the conditioned medium was consistently higher with AT2-null fibroblasts than with wild-type fibroblasts. These results imply that the AT2 receptor negatively regulates the level of active TGF-beta and thus increases NNK-induced lung tumorigenesis. The AT2 receptor function in lung stromal fibroblasts may be a potential modulator of tumor susceptibility in chemical carcinogen-induced lung tumorigenesis.

Angiotensin II Type 2 Receptor Blockers↗
PubMed1989

Nitrosamine metabolism in protein-deficient weanling rats during the process of repletion.

The metabolism of N-nitrosodimethylamine (NDMA) during a 5- to 10-day process of 20% protein repletion was investigated, in vitro and in vivo, in male weanling albino Wistar rats acutely and chronically deprived of protein by feeding, respectively, diets containing no protein or 3.5% for 7 days and one with 3.5% protein for 35 days. Results of experiments using the 5-day rehabilitated animals showed that rate of NDMA demethylation by liver microsomal preparation was 3-fold higher in the chronically protein-dependent animals but comparable between control animals and the more acutely deprived species. In addition, urinary excretion of an oral dose of 40 mg NDMA/kg was significantly less in the chronically protein-dependent animals, which also cleared the blood of an intravenous dose of 5 mg NDMA/kg more rapidly. NDMA metabolism was comparable in all animal groups after 10 days of protein replection.

Animals↗