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At least 1,189 records · Page 66Linked to original sources
PubMed1987

Scanning electron microscopy of changes in the urinary bladder in dogs treated with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN).

The fine structures of the bladder mucosa during BBN carcinogenesis and of bladder tumors induced by BBN in dogs were examined by scanning electron microscopy. Normal dog bladder mucosa was covered with polygonal superficial cells with peaked microridges, but no microvilli. Microridges and uniform microvilli were observed in hyperplastic mucosa. In low grade papillary tumors induced by low doses of BBN, pleomorphic microvilli predominated. In dogs which received high doses of BBN, bizarre pleomorphic microvilli and blebs were observed in papillary lesions, whereas bumpy surfaces with thick short microvilli were observed in non-papillary lesions. These sequential changes which were observed in dog bladder mucosa during BBN carcinogenesis parallelled the changes that occurred in the process of chemical carcinogenesis in rodents, and dog bladder tumors were similar to those of rodents and of human bladder cancers.

Animals↗
PubMed1976

Structural limits of specificity of methylcholanthrene-repressible nitrosamine N-dealkylases. Inhibition by analog substrates.

The dealkylation of dimethyl-, diethyl- and dipropylnitrosamine by hepatic microsomes of Sprague-Dawley rats is repressed by pretreatment of the animals with 3-methylcholanthrene (MC), and this repression progressively decreases with the increase of alkyl chain length. In contrast to its effect on the demethylation of dimethylnitrosamine (DMN), in vivo phenobarbital induces rather than represses the deethylation of diethylnitrosamine. The rates of demethylation of the DMN analog substrates (dimethylformamide, dimethylacetamide, dimethylpropionamide, and dimethylbutyramide), although low as compared to DMN, increase with the acyl chain length. These analogs are potent in vitro inhibitors of Dmn demethylation when used in combination with DMN as substrates, and the inhibition decreases with the length of the acyl chain. Dimethylaminoacetone, which corresponds to the insertion of a CH2 group between the N atom and the carbonyl group in dimethylacetamide, is not an in vitro inhibitor of DMN demethylation; the demethylation rates are additive when theis compound is used as substrate in combination with DMN. The rate of demethylation of dimethylaminoacetone is substantially higher than the rates of the dimethylacylamides, and is significantly repressed by MC-pretreatment. The rate of demethylation of methylphenylnitrosamine is not influenced by MC-pretreatment; the compound is, however, a potent inhibitor of demethylation when used as substrate in combination with DMN. The demethylation rates of 1,1-dimethylhydrazine (the reduction product of DMN) and dimethylaniline are not influenced by MC-pretreatment; neither do they affect the overall rate of demethylation when used as substrate in combination with DMN.

Animals↗
PubMed1976

Transplacental effects of nitrosamines in Syrian hamsters: I. Dibutylnitrosamine and nitrosohexamethyleneimine.

The transplacental carcinogenic effects of dibutylnitrosamine (DBN) and nitrosohexamethyleneimine (N-6-MI) were examined in Syrian hamsters. A proportion of both substances reached the fetal tissue unaltered. No macroscopic malformations were observed in the offspring; however, postnatal mortality was high. Respiratory tumours were found upon histologic examination of surviving animals. Single doses of 30 mg/kg body weight (b.w.) DBN and 2 doses of 10 mg/kg b.w. N-6-MI did not induce tumours in the P-generation, but led to a low tumour incidence in the F1-generation (DBN, 7.0%, N-6-MI, 2.0%). Treatment for up to eight days during the second half of pregnancy led to a higher tumour incidence in the P-generation (DBN, 22%; N-6-MI, 20%), than in the F1-generation (DBN, 6.0%; N-6-MI, 10%).

Animals↗
PubMed1976

Metabolism of nitrosamines in vivo. V Investigation on 14CO2 exhalation, liver RNA labelling and isolation of two metabolites from urine after administration of [2, 5-14C-]dinitrosopiperazine to rats.

The synthesis of N, N'-dinitrosopiperazine and N-nitrosopiperazine, both 14C-labelled in the 2-and 5-position is described. After i.p. application of 10 mg/69.5 muCi/kg[2, 5-14C]-N, N'-dinitrosopiperazine to rats no labelled 7-methylguanine was detected in the liver RNA; 1% of the radioactivity was exhaled as 14CO2, 1% excreted via the bile and about 40% excreted in the urine. Two of the urine metabolites were identified as 3-hydroxynitrosopyrrolidine and 1-nitrosopiperazinone-(3).

Animals↗
PubMed1977

Transplacental effects of nitrosamines in Syrian hamsters. II. Nitrosopiperidine.

Nitrosopiperidine (NP) was found in Syrian hamsters quantitatively in the maternal blood for more than 8 h after subcutaneous injection, whereas it disappeared from placenta, fetus and amniotic fluid within the same time period. For N6MI, only traces were seen after 2 h in the same tissues. The long-term transplacental effect of a single dose of NP was weak, as demonstrated by a low respiratory tract tumor incidence (P-generation: 54%, F1- generation: 4%). Some tumors occurring in the digestive tract of exposed young were not found in their mothers and not commonly observed in controls. These tumors were considered a borderline transplacental effect. Tumors of other sites (i.e., the urogenital and genital tracts, reticuloendothelial system, endocrine organs and other tissues) corresponded in incidences to the overall fluctuations observed in this hamster colony.

Animals↗
PubMed1978

Kinetic studies on the formation of nitrosamines I. Formation of dimethylnitrosamine in aqeous solution of perchloric acid.

The kinetics of nitrosation of dimethylamine (DMA) in aqueous perchloric acid solution have been studied using a differential spectrophotometric technique. The rate law is Initial rate = e[DMA]0 [nitrite]2 0 [H+]/(f + [H+])2 where [DMA]0 and [nitrite]0 represent initial stoichiometric concentrations. At 310.0 K and mu = 2.0 M, e = (2.2 +/- 0.2) X 10(-5) M-1 s-1 and f = (1.28 +/- 0.02) X 10(-3) M. The associated activation energy is 56 +/- 3 kJ mol-1. A clear inhibition of the nitrosation rate by ionic strength has been observed in which only the kinetic parameter (f) has an effective change. It is concluded that under the experimental conditions of this work only the dinitrogen trioxid is the effective carrier for the nitrosation.

Dimethylnitrosamine↗