Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Urethane”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed1994

At least four genes and sex are associated with susceptibility to urethane-induced pulmonary adenomas in mice.

Susceptibility to urethane-induced lung adenomas in mice has a polygenic mode of inheritance, with no obvious discontinuity in lung tumour counts among 37 AXB recombinant inbred strains. However, mean tumour counts were markedly higher in strains carrying the A/J allele at the Kras2 and H2 complex than in those carrying the C57BL/ allele. In 162 F2 hybrids and small numbers of both backcrosses between strain A/J (susceptible) and C57/BL/6 (resistant) mice, five factors influencing susceptibility were identified. Variation due to the 'major' Kras2 locus (chromosome 6) accounted for 60% of the total variation. 'Minor' loci linked to microsatellite markers Tnfb (in the H2 complex), D9Mit11 and D19Mit16 (on chromosomes 17, 9 and 19, respectively) accounted for a further 13% of the variation, and males had more tumours than females with sex differences accounting for 2% of the variation. No significant association with 32 other loci was detected. On a square-root transformed scale, heterozygotes at all marker loci were of intermediate susceptibility compared with homozygotes. The three minor loci and sex only affected lung tumour counts when at least one susceptible Kras2 allele was present.

Adenoma↗
PubMed2001

Facile metal-assisted hydrolysis of a urethane.

Kinetic studies demonstrate that it is possible to achieve large rate enhancements (2 x 10(4)) for the hydrolysis of a urethane group by using metal-bound water or hydroxide as the nucleophile. [reaction: see text]

Hydrolysis↗
PubMed2003

Simple and stereospecific homologation of urethane-protected alpha-amino acids to their higher homologs using HBTU.

A simple, efficient and stereospecific approach for the homologation of urethane-protected alpha-amino acids to beta-amino acids by the Arndt-Eistert method employing Fmoc-/Boc-alpha-amino acid and 2-(1H-benzotriazole-1-yl)-1,1,3,3-tetramethyl-uronium hexafluorophosphate mixture for the acylation of diazomethane synthesizing the key intermediates Fmoc-/Boc-alpha-aminodiazomethanes as crystalline solids is described.

Amino Acids↗
PubMed1973

Immunogenicity and immunosensitivity of urethane-induced murine lung adenomata, in relation to the immunological impairment of the primary tumour host.

The depression of the immunological status of BALB/c mice treated during infancy with two different doses of urethane, alone or combined with cortisone, was evaluated by counting the number of plaque forming cells at 30 or 50 days of age. The incidence of lung adenomatous nodules was directly related to the degree of immunological impairment at 50 days of age. Twenty-seven lung adenomata were tested in an in vitro system involving spleen cells immune against the same single tumour used as target cell. Eighty-six per cent of tumours in the most immunodepressed group of mice were positive compared with 20-40% in the less immunodepressed groups. Syngeneic cross-reaction tests showed that non-immunogenic tumours were immunosensitive since 66% positive tests were obtained when target cells belonging to the less immunodepressed groups were tested with spleen cells of mice immunized with immunogenic adenomata.

Adenoma↗
PubMed1974

Increased incidence of urethane induced lung adenomata by autosensitized lymphocytes.

The present work investigates the influence of autosensitized lymphocytes on the carcinogenic response of the host. Urethane treated SWR mice received 6 fortnightly injections of lymphocytes sensitized in vitro against syngeneic fibroblasts. An increased incidence of lung adenomata was found in these mice compared with controls injected with unsensitized lymphoid cells or with lymphoid cells sensitized against unrelated transplantation antigens. Autosensitized lymphocytes also modified the response of host lymphoid cells to concanavalin A or to stimulation in a mixed lymphocyte culture assay. These results indicate that autoimmune lymphocytes may increase susceptibility of a host to the induction of tumours.

Adenoma↗
PubMed1977

Cell kinetics of urethane-induced murine pulmonary adenomas: III. Implications of the disparity between the rates of entry into DNA synthesis and into mitosis.

Metaphase arrest by vincristine in urethane-induced murine pulmonary adenomas became linear after an interval of 60 min. The rate of entry into metaphase was 0-191%/h, which was considerably less than the 1%/h for the rate of entry into DNA synthesis obtained previously by double labelling. The duration of prophase plus metaphase was calculated to be 1-7 h. A growth fraction of 9% and a cell-loss factor of 52% were derived. The disparity between rates of entry into DNA synthesis and into metaphase was investigated by microdensitometry on Feulgen-stained squash preparations of tumours of varying ages. Tne DNA profiles showed an increasing frequency of hyperdiploid nuclei with age. Circumstantial evidence for polyploidy was provided by the presence of many binucleate cells in the tumours. By analogy with the liver, these cells may well represent a stage in the development of polyploidy, and the possible relevance of these findings to the neoplastic process is considered.

Adenoma↗
PubMed1977

Effect of inhaled plutonium dioxide on development of urethan-induced pulmonary adenomas.

Mice were exposed to plutonium dioxide (PuO2) aerosols 2 weeks before or after urethan injection. Both exposures reduced the number and size of adenomas. The incidence of arrested metaphases showed no consistently significant differences between plutonium-exposed and mock-exposed animals. The results are discussed in relation to recent electron microscopic evidence of degenerative changes in the type II epithelial cells of the mouse lung following PuO2 inhalation. It is concluded that damage at the cellular level may account for the observed reduction in growth of pulmonary adenomas in mice whose lungs contained plutonium particles.

Adenoma↗
PubMed2001

Inhibitory action of nociceptin/orphanin FQ on functionally different thalamic neurons in urethane-anaesthetized rats.

1. In this study we administered nociceptin/orphanin FQ (NC) ionotophoretically onto neurons located in functionally distinct thalamic structures of urethane-anesthetized rats. Extracellular single unit recordings were made in the medial and lateral ventroposterior nucleus, posterior thalamic nucleus, zona incerta, lateral posterior nucleus, laterodorsal nucleus, ventrolateral nucleus and reticular nucleus. 2. NC decreased the firing rate in 60% of thalamic neurons. This decrease in firing rate was accompanied by a significant reduction in the number of high threshold bursts. 3. In about 20% of the neurons NC increased the firing rate. In most cells NC-induced increases in discharge rate could be blocked by the GABA(A) receptor antagonists bicuculline and SR 95531. 4. The NC receptor ligands [Phe(1)Psi(CH(2)-NH)Gly(2)] nociceptin(1-13)NH(2), Ac-RYYRIK-NH(2) and [Nphe(1)]NC(1-13)NH(2) were also evaluated. All these peptides inhibited NC-induced changes in firing rate. In addition, in some neurons where NC inhibited firing, [Nphe(1)]NC(1-13)NH(2) and Ac-RYYRIK-NH(2) elicited per se an increase in firing rate, suggesting the existence of tonic innervation of thalamic neurons by NC-containing fibres. 5. In NC-inhibited neurons nocistatin induced a significant increase in firing rate. 6. The present study demonstrated that NC regulates various thalamic nuclei related not only to somatosensory, but also to the visual and motor functions.

Action Potentials↗
PubMed1977

Protein phosphorylation in normal and neoplastic development. Cyclic AMP-dependent protein kinase activity in urethane-induced pulmonary tumours.

The cyclic AMP-dependent protein kinase specific activities of cytosol fractions from urethane-induced lung tumours and from normal mouse lung were determined. Both basal and cyclic AMP-stimulated activities in tumours were twofold higher than those of normal lung. Since neonatal and adult lung cytosols have identical kinase activities, the high activity in tumours appears to be a tumour-specific property.

Animals↗
PubMed2001

Delayed-type hypersensitivity and humoral immunity modulation by dietary lipids in a murine model of pulmonary tumorigenesis induced by urethan.

Mice fed on semisynthetic formulas containing 15% of corn oil (CO), cod fish liver oil (FO), oleic acid (O) or a mixture of 46% of palmitic and 50% of stearic acids (PS) were treated with urethan during 18 weeks for lung tumor induction. Delayed-type hypersensitivity (DTH) assay, hemagglutination assay and the amount of lung nodes (alveolar adenocarcinomas) were recorded. Results showed significantly greater DTH in CO and FO with respect to O and PS feeding mice; the two last ones induced an essential fatty acid (EFA) deficiency (EFAD). In the O lot there was a non-significant diminution of the humoral response. EFAD animals exhibited a tendency to increase number of lung nodes in relation to CO and FO lots. Splenomegalia was recorded in FO lot. Confront between spleen weight and DTH showed a 72% correlation, suggesting an increase in cellular immunity as increasing unsaturation. It may be concluded that in this suitable model of tumorigenesis the manipulation of dietary lipids may be a strategy to modify the immune system response.

Adenocarcinoma↗
PubMed1952

The enhancing effect of urethane on the severity of infection with pneumonia virus of mice.

Urethane, given parenterally or orally to mice, increased the severity of PVM infection. Not only were the lesions more extensive but mice could be infected with smaller inocula of virus and the multiplication of virus in the lung was enhanced. There was atrophy of lymphoid tissues but no suppression was noted of antibody formation. No relation could be found between PVM infection and the development of pulmonary adenomas in mice.

Animals↗
PubMed1989

Enhanced malignant phenotype of urethane-induced lung adenoma associated with sialoadenectomy in BALB/c mice.

Mouse lung adenoma were induced in adult female BALB/c mice by chronic i.p. urethane injection. Sialoadenectomy of the mice prior to carcinogen treatment did not alter the frequency or size of lung adenoma. However, sialoadenectomized mice exhibited a decrease in the proportion (18 versus 52%) of tumours which exhibited a low nuclear to cytoplasmic ratio and which grew along alveolar septa. Sialoadenectomy was also related to a complementary increase in the proportion (82 versus 48%) of tumours with large vesicular nuclei, prominent nucleoli and generally increased phenotypic features of malignancy. Replacement of epidermal growth factor (EGF) in sialoadenectomized mice restored the tumour-type ratio observed in non-sialoadenectomized mice. These data are discussed with respect to the possible roles of EGF in mouse lung alveologenic carcinoma formation and the cell type of origin for the tumours observed.

Adenoma↗
PubMed1994

The effect of pyridine on the in vitro and in vivo metabolism of ethyl carbamate (urethane) by rat and mouse.

Ethyl carbamate (EC, urethane) is a known carcinogen in laboratory animals. A genotoxic mechanism has been proposed which involves the bioactivation of EC to a reactive epoxide by the ethanol-inducible CYP2E1. The purpose of this study was to determine if pyridine (200 mg/kg i.p.), an inducer of CYP2E1, would increase the in vitro metabolism of EC and the in vivo binding of EC to cellular macromolecules. Treatment of rats or mice with pyridine increased hepatic microsomal metabolism of [14C-carbonyl]EC to CO2, but had little effect on pulmonary microsomal metabolism. The increase in hepatic metabolism was inhibited by the CYP2E1 inhibitor diethyldithiocarbamate, but not by the esterase inhibitor paraoxon, clearly indicating a role for this isozyme in hepatic metabolism of EC. In vivo, pyridine (200 mg/kg i.p.) administered 18 h prior to dosing with EC decreased the binding of [14C-ethyl]EC to cellular macromolecules. These data indicate that pyridine administration to rats and mice induces CYP2E1 metabolism of EC in vitro, but inhibits EC metabolism in vivo, perhaps by acting as an alternate substrate for CYP2E1.

Animals↗
PubMed1996

Detection of 1,N6-ethenodeoxyadenosine and 3,N4-ethenodeoxycytidine by immunoaffinity/32P-postlabelling in liver and lung DNA of mice treated with ethyl carbamate (urethane) or its metabolites.

The capacity of the chemical carcinogen ethyl carbamate (EC, urethane) and its metabolites vinyl carbamate (VC) and vinyl carbamate epoxide (VCO) to form ethenobases was studied in liver and lung DNA of 12-day-old and adult CD-1, B6C3F1, C3H/HeJ and C57BL/6J mice. Following single and multiple doses of EC, VC or VCO, the formation of 1,N6-ethenodeoxyadenosine (epsilon dA) and 3,N4-ethenodeoxycytidine (epsilon dC) was quantified by an immunoaffinity chromatography/32P-postlabelling technique. Both etheno adducts were detected in untreated control DNA samples from liver and lung in the range of 2-15 adducts/10(9) parent nucleotides. Following five repeated injections of 250 or 280 nmol/g body wt VC to adult mice, 51, 57 and 78 epsilon dA/10(9) dA and 28, 42 and 42 epsilon dC/10(9) dC (means of duplicate analyses) were detected in liver DNA of CD-1, C3H/HeJ and C57BL/6J mice respectively. In lung DNA of these VC-treated mice, the levels were 87, 49 and 58 (epsilon dA/10(9) dA) and 64, 39 and 43 (epsilon dC/10(9) dC) respectively. Under similar dose regimens, lower levels of etheno adducts were detected in B6C3F1 mice. Etheno-DNA adducts were also formed in liver and lung upon treatment with EC in adult mice, but at 3-fold lower levels as compared with VC. In 12-day-old C3H/HeJ and C57BL/6J mice, 2- to 3-fold higher etheno adduct levels were detected in liver DNA, when compared with adults, upon a single treatment with 250 nmol/g body wt VC, suggesting that young animals are more susceptible to adduct formation. Combined analysis of adduct formation in adult CD-1, C3H/HeJ and C57BL/6J mice at the higher dose showed a statistically significant increase in etheno adduct formation in the order EC > VC. The results demonstrate that EC and its activated intermediates bind to liver and lung DNA to form epsilon dA and epsilon dC, and the differences in DNA binding further support the hypothesis that metabolic activation of EC to VC is involved. Preliminary data also suggest that background levels of epsilon dA and epsilon dC in DNA are affected by the type of diet given to the animals.

Animals↗
PubMed1985

Susceptibility to urethan-induced pulmonary adenomas between A/J and C57BL/6J mice: use of AXB and BXA recombinant inbred lines indicating a three-locus genetic model.

For insight into the number of genes governing differential susceptibility such as in mice of the inbred strain A/J (A) highly susceptible to the induction of pulmonary adenomas by urethan in comparison to resistant strain C57BL/6J (B6) mice, tumor induction was studied in the AXB and BXA series of recombinant inbred (RI) strains derived respectively from A female X B6 male and B6 female X A male ancestral lines. Mice from 46 of these lines were given injections with 1 mg urethan/g (body wt), and the tumor number was assessed 4 months later. Lung tumor multiplicity for several RI lines was independently characterized in the Boulder, CO, and Montreal laboratories, and very similar numbers were obtained. Most lines had multiplicities intermediate to those of the progenitor strains, clearly indicating that more than a single gene accounted for the differences in lung tumor susceptibility between A and B6. The tumor incidence and multiplicity data fit very closely to what would be expected under a three-locus model, and we designated these genes "Pas" for pulmonary adenoma susceptibility. One locus called "Pas-1" had an effect on tumor multiplicity greater than that of the other loci.

Adenoma↗
PubMed1991

Propofol modification of evoked hippocampal dentate inhibition in urethane-anesthetized rats.

To learn more about the site and mode of action of propofol, the authors anesthetized rats with urethane, and implanted a stimulating electrode in the perforant pathway and a recording electrode in the hippocampal dentate gyrus to measure evoked field responses. Catheters were placed in the jugular vein and carotid artery to measure blood pressure, take blood samples for measurement of blood gases, and inject drugs. Rat lungs were ventilated, and increasing doses of propofol or its 10% fat emulsion vehicle were administered. Over a dose range of 2.5-40 mg/kg, propofol had little effect on the field excitatory postsynaptic potential (EPSP) or the field population spike (PS), suggesting no important actions on perforant pathway fibers or intrinsic granule cell excitability. With the use of various paired-pulse stimulation paradigms, it was demonstrated that propofol administration led to a dramatic decrease in granule cell excitability over interpulse intervals of 10-100 ms. The magnitude of this effect clearly was related to dose, and the effect was reversible with discontinuance of drug. The vehicle had marginal effects on granule cell excitability. These were significantly less than those produced by propofol. Transient reductions in blood pressure followed by transient increases to above baseline were observed after administration of propofol at most doses. Increased heart rates accompanied the slight increase in blood pressure. Except at the largest dose of propofol tested, cardiovascular measures had returned to near control levels by 8 min, when the evoked potentials were evaluated. Arterial blood gases showed little change throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗