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PubMed1979

[Studies on growth hormone secretion in starved rats under urethane anesthesia (author's transl)].

Adult male wistar rats averaging 200 g each were subjected to food removal for 1--6 days or fed ad libitum throughout (controls). Plasma GH levels and pituitary GH contents were measured by radioimmunoassay. The GH responses to intravenous injection of TRH (2.5 microgram/100 g B.W.), PGE1(5 microgram/100 g B.W.), LH-RH (1 microgram/100 g B.W.) and Chlorpromazine (CPZ, 100 microgram/100 g B.W.) were tested under urethane anesthesia. Circulating GH levels were significantly increased by prolonged starvation, while pituitary GH contents progressively decreased with increased periods of starvation. In addition, following the TRH administration, plasma GH levels increased in starved rats compared to the control rats. A similar effect was also observed with PGE1. In contrast, the administration of CPZ, which was reported to act at the hypothalamic level, failed to potentiate GH release in starved rats under urethane anesthesia. These observations suggest an increased susceptibility of starved rats to urethane anesthesia with the administration of TRH and PGE1 in the GH secretory mechanism. In addition, the fact that no further potentiation of GH release was observed by CPZ treatment may indicate an abnormality of the hypothalamic dopaminergic mechanism in starved animals.

Anesthesia↗
PubMed2002

Sleep-time variation for ethanol and the hypnotic drugs tribromoethanol, urethane, pentobarbital, and propofol within outbred ICR mice.

To evaluate the phenotypic variation within a commercial outbred mouse stock, we examined sleep-time (or duration of loss of righting reflex) of outbred ICR mice after i.p. injection of ethanol (4.0 g/kg of body weight), urethane (1.3 g), tribromoethanol (250 mg), and pentobarbital (60 mg), and after i.v. injection of propofol (30 mg). We observed high-grade individual differences in sleep-time that ranged from 0 to 179 min, 83.1 +/- 4.3 (mean and SEM of 100 mice) for ethanol; 0 to 169 min, 64.5 +/- 3.1 for pentobarbital; 0 to 160 min, 36.6 +/- 3.6 for urethane; 0 to 120 min, 21.5 +/- 2.2 for tribromoethanol; and 3 to 20.5 min, 7.1 +/- 0.3 for propofol. This extensive phenotypic variance within the outbred stock was as great as the variation reported among inbred strains or selected lines, and the varied susceptibility within the colony was inherited by Jcl:ICR-derived inbred strains IAI, ICT, IPI, and IQI. The range of sleep-time variance for ethanol, pentobarbital, urethane, tribromoethanol, and propofol within four-way cross hybrid Jcl:MCH(ICR) mice was 86.6%, 63.3%, 124%, 61.0%, and 53.1% that of outbred Jcl:ICR mice, respectively. The present study indicates that phenotypic variance within an outbred Jcl:ICR stock was at high risk for susceptibility to the drugs that depress the central nervous system and that Jcl:ICR-derived inbreds may be an excellent source of animal models for studying the anesthesia gene.

Animals↗
PubMed1985

Conditioning-related single unit activity in the frontal cortex of urethane anesthetized rats.

Responses of frontal cortex single units to a tone preceding medial forebrain bundle (MFB) stimulation were recorded in urethane anesthetized rats. The animals were implanted with monopolar electrodes for MFB stimulation and, following recovery, stimulation parameters which supported self-stimulation were determined for each rat. Prior to the unit recording experiment, the animals were trained to associate a 2-sec tone with MFB stimulation. Trials were presented at variable intervals. Under urethane anesthesia, single units were isolated and the responses of units to paired and unpaired tones were determined. The results indicate that conditioning-related responses of frontal cortex single units can be recorded in urethane anesthetized rats.

Anesthesia, General↗
PubMedDate not supplied

Expression of the glucocorticoid receptor and K-ras genes in urethan-induced mouse lung tumors and transformed cell lines.

Glucocorticoids influence cell proliferation and differentiation in the lung. We examined the expression of the glucocorticoid receptor (GR) gene in urethan-induced mouse lung tumors and transformed lung cell lines to determine whether any altered responsiveness to these steroids is involved in the neoplastic development of some lung tumors. We find that a GR mRNA of similar size and amount is expressed in both normal lung and urethan-induced lung tumors. The K-ras gene is activated in urethan-induced lung adenomas and transformed lung cell lines. Both alveolar and papillary lung adenomas express slightly elevated levels of K-ras mRNA and similar levels of H-ras mRNA, but variable levels of c-myc mRNA, GR and K-ras mRNAs are concurrently expressed in a cyclic manner during the proliferation of nontransformed C10 and transformed A5 lung cell lines. Treatment of the C10 cells with dexamethasone (Dex) results in the inhibition of cell proliferation and the down-regulation of both the GR and K-ras mRNA. Dex treatment also down-regulated GR mRNA levels in A5 and LM2 cells, but no inhibitory effect was observed on K-ras mRNA levels or cell proliferation. These results suggest that glucocorticoids can inhibit K-ras expression in nontransformed lung cells. Although transformed lung cells respond to the steroid by down-regulation of the GR, the presence of an activated K-ras allele may override the inhibitory effects of these hormones on cell proliferation.

Animals↗
PubMed1998

Blood flow rate in normal and tumor-bearing rats in conscious state, under urethane anesthesia, and during systemic hypothermia.

The blood flow rates of 14 tissues in the body were determined by microsphere method using normal and tumor-bearing rats kept conscious or under urethane anesthesia. The effects on the blood flow rate in the tissues were assessed for multimodal therapy, systemic hypothermia for ischemic brain injury, and local hyperthermia and angiotensin II-induced hypertensive chemotherapy for cancer. Urethane anesthesia showed no effect on cardiac output, while there was a tendency of decrease of blood flow rate and % of cardiac output in each tissue other than muscle tissue, in which they increased as a counterbalance, in normal and tumor-bearing rats. Systemic hypothermia gave results similar to those of urethane anesthesia in normal rats, but for tumor-bearing rats, it decreased cardiac output, and consequently the blood flow rate in most tissues. Brain blood flow rate was about half of that in the conscious rats. Local hyperthermia also decreased the cardiac output and blood flow rate in each tissue, including the tumor tissue. Angiotensin II-induced hypertension showed no effect on cardiac output, had various effects on blood flow rate in each tissue, and led to no increase in the tumor blood flow rate. Simulations based on the physiological pharmacokinetic modeling suggested that intramuscular injection of a lung-specific derivative of ceftazidime would provide the ideal biodistribution to ensure its optimal therapeutic efficacy during systemic hypothermia. This methodology, namely the pharmacokinetic simulation based on the physiological values of the body, will provide a useful piece of information on drug delivery systems under various conditions.

Anesthesia, Intravenous↗
PubMed1999

[Search for Ki-ras codon 61 mutations in lung adenomas induced in neonatal BALB/c mice with 5-bromodesoxyuridine injection followed by urethane treatment].

BALD/c mice were injected, s.c., 1 mg 5-bromodeoxyuridine (BDU) on days 1.3 and 7 after birth and/or 0.1 ml 5% solution of urethane, 5 times a day every fourth day, i.p., at the age of 3 months. Lung tumors, mostly adenomas, developed in 67% of males and 56% of females, treated with urethane alone. Tumor frequency in response to BDU + urethane rose to 91% in males and 56% in females; multiple neoplasia increased too. In BDU-treated animals, lung tumors appeared in 13% of males and 25% of females whereas in intact controls-3 and 11%, respectively. DNA isolated from paraffin mounts of tumor tissue was used to identify mutations in codon 61 of Ki-ras oncogene. Polymorphism studies of restriction fragment lengths in PCR products failed to detect CAA CTA and CAA CGA sequence changes in 7 samples of DNA. Our findings do not rule out other mutations of RAS oncogenes in our material. They also suggest that further research focus on Ki-ras codon 12 as well as Ha-ras "hot" triplets.

Animals↗
PubMed2000

The effect of exposure to a commercial 2,4-D herbicide formulation during gestation on urethan-induced lung adenoma formation in CD-1 mice.

Female CD-1 mice were exposed to a commercial amine formulation of 2,4-dichlorophenoxyacetic acid (2,4-D) on days 6-16 of gestation in drinking water at concentrations ranging from 0 to 1.0% of the formulated product, equivalent to approximately 0-650 mg/kg/d expressed as the amine derivative. The effect of 2,4-D on urethan-induced pulmonary adenoma formation was evaluated in female offspring 19 w after birth. Urethan-induced sleeping times observed following ip injection of 1.5 mg urethan/g bw 7 w after birth were not altered by 2,4-D (p = 0.10), indicating that 2,4-D did not affect the rate of urethan elimination. 2,4-D exposure did not affect the number of tumors produced (p = 0.58), but did reduce the mean tumor diameter in the highest dose group (p < 0.01). This minor antineoplastic activity of 2,4-D may be related, in part, to inhibitory effects of 2,4-D on various enzymatic or metabolic pathways, essential for cellular growth and tissue development. Since exposure to 2,4-D during pregnancy had little impact of tumor production, it is unlikely that persistent alteration to developing immune cells involved in the cell-mediated immunosurveillance mechanisms occurred. The subtle alteration in tumor size and the mild impairment of growth in the offspring were observed almost exclusively in the highest treatment group. Since this level of exposure is well in excess of those associated with normal application of 2,4-D, the hazard to non-target mammalian populations appears minimal.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1976

Relationship between nucleolar microspherule formation by urethan and inhibition of RNA and protein synthesis.

Liver tissues of suckling C3Hf mice treated with urethan, a carcinogen and inhibitor of RNA synthesis, and with cycloheximide, an inhibitor of protein synthesis, were studied by electron microscopy and by light microscope radioautography. At 4 and 12 hr after treatment with a single dose of urethan (1 mg/g body weight). [3H]uridine incorporation in hepatocyte nuclei was 38 and 9% lower than in controls and became 32% higher at 24 hr. Nucleolar microspherules were found 1.5 and 4 hr after the treatment, increased considerably in number at 10 and 12 hr, and decreased at 24 hr. These results suggest an inverse relationship between RNA synthesis and formation of microspherules. Cycloheximide alone (3 mg/kg body weight) produced microspherules, whereas in combination with a dose of 1 or 2 mg of urethan per g body weight it partially prevented or potentiated, respectively, the microspherule production.

Animals↗
PubMed1976

[Epithelial proliferations in organ cultures of mouse lung treated with urethane and 3,4-benzopyrene].

The authors carried out some series of experiments under the conditions of organ cultures of lungs of mice, treated with urethane and 3,4-benzpirene. They succeeded lung culturinf up to 14-th and 21-th day. Growths of bronchial and bronciolar epithelium manifested at various degree were obtained in the lung extracts from mice, treated with urethane and 3,4-benzpirene. The most manifested proliferation was observed in extracts, treated with urethane at a dose of 10 mg/ml and 3,4-benzpirene -- 64 gamma/ml.

Animals↗
PubMed1992

[Carcinogenesis induced by the neonatal administration of 5-bromo-2'-deoxyuridine (BUDR) and subsequent exposure to urethane in BALB/c mice].

Male and female BALB/c mice were subcutaneously injected with 1 mg 5-bromo-2'-deoxyuridine (BDU) on days 1, 3 and 7 after birth and/or given 0.1 ml 5% urethane solution 5 times every 3 days starting at the age of 3 months. Treatment with BDU alone was followed by retardation of growth, loss of body weight and liver mass but had no significant impact on tumor occurrence. Combined application of BDU and urethane was found to potentiate the effect of the latter agent resulting in an increase in the occurrence and multiplicity of lung adenoma. Male mice treated with the above combination showed a significantly higher occurrence of lung adenocarcinoma and hemoblastoses as compared to the other animal groups. It is suggested that genome instability caused by neonatal BDU treatment potentiates the carcinogenic effect of urethane.

Animals↗
PubMed2006

[Melatonin inhibits urethane-induced carcinogenesis tumors in murine lung].

Non-inbred SHR/u 3-month old mice were injected a single dose of urethane 1 g/kg, intraperitoneally. Beginning from day I after injection, they received melatonin 20 mg/l or 2 mg/l with drinking water at nighttime. After 28 days of the experiments, mice were sacrificed, lung adenomas counted and examined morphologically. Samples of blood and ling tissue were taken from each group and assayed for malonic dialdehyde (MDA) and catalase level. Tumor count of lung adenomas in the untreated group (control) was 23 +/- 2.63, melatonin 20 mg/l--14 +/- 1.2 (p < 0.01) and melatonin 2 mg/l--11 +/- 0.72 (p < 0.01). Urethane-treated mice revealed increased levels of MDA (62%) and catalase (70.7%) in blood-serum and in lung tissue (36.5%) as compared with control. Melatonin treatment significantly lowered concentrations of MDA in blood-serum and catalase (blood-serum and lung) rather than in the lung bearing urethane-induced tumor. Antitumor and antioxidant effect of relatively low dosage of melatonin appeared to be more effective than those of a larger one.

Adenoma↗
PubMed1976

C-type virus particles in urethan-induced pulmonary and renal carcinomas, in cell-graft-transmitted carcinosarcomas, and in filtrate-induced lymphomas in mice.

Repeated injections of urethan into suckling BALB/c mice induced multiple papillary adenocarcinomas in the lungs and kidneys. When the pulmonary tumors were transplanted i.p. by cell graft into 6 suckling BALB/c mice, they induced disseminated carcinosarcomas within the peritoneal cavity in all inoculated animals. Tumors resulting from the transplantation of tumor cells were used for preparation of filtered extracts. The filtrates were inoculated into 6 suckling BALB/c mice and induced generalized malignant lymphomas in all animals. The primary urethan-induced pulmonary and renal tumors, the carcinosarcomas that resulted from i.p. cell transfer, and also the generalized malignant lymphomas induced by inoculation of filtered extracts contained C-type virus particles. Theoretically, it could be assumed that both the primary urethan-induced pulmonary and renal tumors, as well as the cell-graft-induced peritoneal carcinosarcomas, contained the C-type virus particles as passengers, not necessarily related etiologically to the tumors in which they were found. It is quite likely, however, that these virus particles were etiologically related to the filtrate-induced malignant lymphomas in which they were also found.

Adenocarcinoma, Papillary↗
PubMed1991

Alterations in glial cell morphology and glial fibrillary acidic protein expression in urethane-induced retinopathy.

Urethane injection in newborn rats causes a photoreceptor degeneration without initial damage to the retinal pigment epithelium, choriocapillaris, or inner retina. In later stages, retinal vessels become incorporated into the retinal pigment epithelium (RPE) and change from a continuous endothelial cell phenotype to a fenestrated phenotype. At the light-microscopic level, there do not appear to be morphologic changes in the inner retina up to 24 weeks of age. Ultrastructurally, however, there are alterations in Müller cell cytotopographic organization. In the normal retina, intermediate filaments are primarily found from the ganglion cell layer to the inner nuclear layer. These filaments do not show glial fibrillary acidic protein immunoreactivity (GFAP-IR) in the normal animal. In the urethane-treated animals, the compartmental organization of the Müller cell organelles is moved vitread. Intermediate filaments are found in the end-foot region, and in the inner plexiform layer, bundles of intermediate filaments become more prominent. All of these filaments are GFAP-IR positive. The new expression of GFAP in the Müller cell may be linked to the observed rearrangement of the cytoskeletal elements. In urethane-induced retinopathy, GFAP-IR is found associated with vessels in all layers of the remaining retina. However, it is not seen accompanying vessels into the RPE. Ultrastructurally, there is no glial investment of the RPE-associated vessels. This absence of glial investment may permit the change in phenotype observed in these vessels.

Animals↗
PubMed1990

Interglial cell gap junctions increase in urethane-induced photoreceptor degeneration in rats.

Gap junctions are found between astrocytes in the inner retina of normal rats, but they are rare between Müller cells or between astrocytes and Müller cells in the inner retina. After photoreceptor degeneration induced by urethane treatment of newborn animals, morphologic alterations of glial cells occur in the inner retina. The Müller cells withdraw from the inner limiting membrane, and the astrocytes hypertrophy and occupy the vitread surface of the inner limiting membrane. The frequency and size of the gap junctions between astrocytes increases with time in rats with urethane-induced photoreceptor degeneration, to a greater extent than expected from elaboration of additional astrocyte plasma membrane. The gap junction-profile length per glial cell membrane-contact length is 2.8 +/- 1.1 microns/1000 microns of membrane in 8-week-old normal animals; it increases to 18.9 +/- 9.4 microns/1000 microns of membrane at 56 weeks of age in urethane-treated animals. The average size of the gap junction-profile length doubles during this same period. To the authors' knowledge this is the first study demonstrating pathologic changes in gap junctions in central nervous system tissue. The authors speculate that this up-regulation of gap junctions occurs in response to an altered extracellular ionic composition in an attempt to increase the lateral spatial buffering of K+ by these cells. The relative location of glial cells in retina can determine, in part, the vulnerability of the retina to edema.

Animals↗
PubMed1987

Effect of red ginseng on natural killer cell activity in mice with lung adenoma induced by urethan and benzo(a)pyrene.

It was previously reported that red ginseng extract inhibited carcinogenesis by urethan, DMBA, and aflatoxin B1 [Yun et al: Cancer Detect Prevent 1983; 6:515-25]. In an attempt to investigate the mechanism of the anticarcinogenic effect of ginseng, the natural killer (NK) activity and the incidence of lung adenoma were followed over a period of 48 weeks postinjection with urethan or benzo(a)pyrene. The NK activity was markedly depressed from 4 weeks to 24 weeks after injection of carcinogens. This decreased NK activity was returned to the level of controls by administration of ginseng. At the same time, a lower incidence of lung adenoma was noted following administration of ginseng to urethan-injected mice. However, the lung adenoma induced by benzo(a)pyrene began to occur at 48 weeks in which NK activity had naturally declined to a level too low to be affected by ginseng, and administration of ginseng did not decrease the incidence. In conclusion, these results suggest that the anticarcinogenic effect of ginseng may be related to the augmentation of NK activity.

Adenoma↗
PubMed1978

[Transplacental effect of urethane on DNA synthesis in mouse embryonal lung tissue during organotypical cultivation].

Kinetics of DNA synthesis was estimated by autoradiography in the organ cultures of murine embryonic lung tissue. Strain A mice were taken for this experiment (intact and exposed to transplacental action of urethane--30 mg/g to a pregnant mouse, subcutaneously, once). The explants were examined 1,7, 15 and 21 days after the cultivation. Transplacental urethane inhibited DNA synthesis the first 24 hours. The label index became approximately 3 times less. The next two days it was restored and then stimulated. The maximal label index was noted in the experimental explants on the 7th cultivation day, i.e. on the 8th-10th day after the transplacental action of urethane on the lung tissue in utero. By the 15th cultivation day the label index dropped but was higher than in the intact explants; by the 21st day DNA synthesis in the intact cultures ceased completely, whereas in the experimental animals--it continued.

Animals↗
PubMed1984

Urethane-induced rat retinopathy. Plasticity of the blood-retinal barrier in disease.

Sodium fluorescein and fluoresceinated dextrans penetrate the blood-retinal barrier (BRB) of rats with urethane-induced retinopathy. We have extended these observations, using horseradish peroxidase (HRP) as an ultrastructural probe of the BRB. Intravenous HRP penetrated the BRB 7 weeks after urethane treatment began. This occurred where retinal capillaries invaded the retinal pigment epithelium (RPE) after photoreceptor degeneration. The penetration intensified with duration of the retinopathy, but remained localized near intraepithelial capillaries. The mechanisms by which HRP penetrated the BRB changed as the retinopathy progressed. In the earliest stages (7-10 weeks of age) vesicular transport across endothelia and/or leakage from the choriocapillaris into the pericapillary space of intraepithelial capillaries and then along this space into the retina. At later stages, two more mechanisms were at work: (1) fenestrae developed in the intraepithelial capillaries, and (2) the RPE attenuated, losing its barrier function. Except where this occurred, intercellular RPE junctional complexes remained intact and retarded HRP. We suggest that the rat urethane retinopathy models the plasticity of BRB components--RPE and endothelia--over the course of retinal disease.

Animals↗
PubMed1984

Enhancement of urethan-induced adenoma formation in Swiss mice exposed to methylmercury.

Female Swiss mice were exposed to methylmercury in the drinking water for 15 weeks. The mice were administered concentrations of methylmercury ranging from 0 to 2.0 micrograms/mL mercury. After three weeks of the 15 week exposure period, the mice were administered urethan (1.5 mg/g) intraperitoneally. Pulmonary adenoma formation was evaluated 12 weeks later. Methylmercury exposures of 0.2 and 0.5 micrograms/mL did not affect the number of adenomas, but 2.0 micrograms/mL mercury caused a significant increase in adenoma production. A dose-dependent increase in the mean tumor diameter was seen at methylmercury exposures up to 0.5 micrograms/mL. No further increase in diameter was seen at higher exposures (2.0 micrograms/mL). The changes in adenoma production were seen at exposure levels of methylmercury which did not cause any clinical manifestations. Animal weight gains and water consumption were not affected. In addition, urethan-induced sleeping times which reflect the rate of urethan metabolism or excretion remained unchanged.

Adenoma↗