Search results for " strain"

showing 10 items of 868 documents

Biological activation of 1,3-butadiene to vinyl oxirane by rat liver microsomes and expiration of the reactive metabolite by exposed rats.

1983

When 1,3-butadiene is incubated with rat liver microsomes and NADPH both enantiomers of vinyl oxirane are formed, the amount of epoxide being dependent on incubation time, microsomal protein, and substrate concentration. Inhibition by SKF 525 A or dithiocarb as well as induction by pretreatment with phenobarbital or 20-methylcholanthrene suggest participation of cytochrome P-450 in this reaction. The amount of epoxide is enhanced by addition of 1,1,1-trichloropropene oxide and reduced by glutathione, especially in the presence of hepatic cytosol. When rats are exposed to 1,3-butadiene in a closed chamber (conditions of maximal metabolism) vinyl oxirane is exhaled and can be quantitatively d…

MaleCancer ResearchCytochromeMetaboliteEpoxideIn Vitro TechniquesAcetonechemistry.chemical_compoundEthers CyclicmedicineButadienesAnimalsBiotransformationbiology13-ButadieneRats Inbred StrainsStereoisomerismGeneral MedicineGlutathioneMetabolismRatsOncologychemistryBiochemistryMicrosomebiology.proteinMicrosomes LiverEpoxy CompoundsPhenobarbitalmedicine.drugMutagensJournal of cancer research and clinical oncology
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RORC1 Regulates Tumor-Promoting "Emergency" Granulo-Monocytopoiesis

2015

Cancer-driven granulo-monocytopoiesis stimulates expansion of tumor promoting myeloid populations, mostly myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs). We identified subsets of MDSCs and TAMs based on the expression of retinoic-acid-related orphan receptor (RORC1/RORγ) in human and mouse tumor bearers. RORC1 orchestrates myelopoiesis by suppressing negative (Socs3 and Bcl3) and promoting positive (C/EBPβ) regulators of granulopoiesis, as well as the key transcriptional mediators of myeloid progenitor commitment and differentiation to the monocytic/macrophage lineage (IRF8 and PU.1). RORC1 supported tumor-promoting innate immunity by protecting MDSCs from …

MaleCancer ResearchMyeloidNeutrophilsMacrophageCellular differentiationApoptosisMonocyteMonocyteshemic and lymphatic diseasesMyeloid CellsSOCS3Myeloid CellMyelopoiesisMice KnockoutMicroscopy ConfocalReverse Transcriptase Polymerase Chain ReactionMedicine (all)NeutrophilCell DifferentiationNuclear Receptor Subfamily 1 Group F Member 3Animals; Apoptosis; Cell Differentiation; Cell Line Tumor; Cytokines; Female; Gene Expression Regulation Neoplastic; Granulocytes; Humans; Immunohistochemistry; Macrophages; Male; Mice 129 Strain; Mice Inbred C57BL; Mice Knockout; Microscopy Confocal; Monocytes; Myeloid Cells; Myelopoiesis; Neoplasms Experimental; Neutrophils; Nuclear Receptor Subfamily 1 Group F Member 3; Reverse Transcriptase Polymerase Chain Reaction; Tumor Burden; Cancer Research; Cell Biology; Oncology; Medicine (all)ImmunohistochemistryTumor BurdenGene Expression Regulation NeoplasticHaematopoiesismedicine.anatomical_structureOncologyCytokinesFemaleMyelopoiesisHumanMice 129 StrainBiologySettore MED/08 - Anatomia PatologicaGranulopoiesisArticleMyelopoiesiCell Line TumormedicineAnimalsHumansCytokineInnate immune systemAnimalMacrophagesApoptosiGranulocyteNeoplasms ExperimentalCell BiologyMice Inbred C57BLImmunologyCancer researchIRF8Granulocytes
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pH distributions in spontaneous and isotransplanted rat tumours.

1988

Spontaneous mammary tumours of the rat with various degrees of malignancy exhibit similar tissue pH distributions. The mean pH (+/- s.d.) of dysplasia is 7.05 +/- 0.20. In benign tumours the mean pH is 6.95 +/- 0.19 and in malignant tumours it is 6.94 +/- 0.19. In contrast, tumours with the same degree of malignancy but different histologies show different pH distributions. Benign tumours with a higher percentage of fibrous tissue exhibit less acidic pH values than those with larger portions of epithelial cells (delta pH = 0.38 pH units). The pH distribution in the benign tumours is independent of the tumour wet weight up to stages of very advanced growth. In the malignant tumours, a trend …

MaleCancer ResearchPathologymedicine.medical_specialtyNecrosisFibrous tissueBiologyMalignancyBenign tumoursmedicinePh gradientDistribution (pharmacology)AnimalsSarcoma YoshidaMammary Neoplasms ExperimentalRats Inbred StrainsHydrogen-Ion Concentrationmedicine.diseaseRatsTransplantation IsogeneicOncologyDysplasiaTumour sizeFemalemedicine.symptomNeoplasm TransplantationResearch ArticleBritish Journal of Cancer
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The rat liver foci bioassay: II. Investigations on the dose-dependent induction of ATPase-deficient foci by vinyl chloride at very low doses

1985

In order to study the dose-dependence of the genotoxic effect of vinyl chloride (VC) hepatocellular ATPase-deficient foci were evaluated after subchronic exposure of newborn rats. Wistar rats were exposed from day 1 after birth over 10 weeks to 10, 40, 70, 150, 500 and 2000 p.p.m. VC (8 h/day; 5 days/week). One week after cessation of exposure hepatic ATPase-deficient foci were quantitated. For a subsequent investigation lower dose range groups of female and male Wistar and Sprague-Dawley rats were exposed (8 h/day; 5 days/week) to 2.5, 5, 10, 20, 40 and 80 p.p.m. VC. Exposure started at day 3 of life and lasted for 3 weeks. After cessation of exposure the animals were maintained for 10 wee…

MaleCancer ResearchPathologymedicine.medical_specialtyVinyl CompoundsATPaseVinyl ChlorideDose dependenceVinyl chlorideAndrologychemistry.chemical_compoundLiver Neoplasms ExperimentalSex FactorsSpecies SpecificitymedicineAnimalsBioassayCarcinogenAdenosine TriphosphatasesDose-Response Relationship DrugbiologyLow doseRats Inbred StrainsGeneral MedicineRatsLinear relationshipLiverchemistryRat liverbiology.proteinBiological AssayFemalePrecancerous ConditionsCarcinogenesis
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The rat liver foci bioassay: I. Age-dependence of induction by vinyl chloride of ATPase-deficient foci

1985

The age-dependence of the induction of pre-neoplastic enzyme-altered hepatic foci was investigated. Rats were exposed (8 h/day, 7 days/week) to 2000 p.p.m. vinyl chloride (VC) either 'transplacentally' (exposure of pregnant females), or immediately after birth for different time intervals (5, 11, 17, 47, 83 days) or from an age of 7 or 21 days onwards. The animals were then kept without further treatment; livers were evaluated for ATPase-deficient foci at the age of 4 months. 'Transplacental' exposure and exposure from day 1 through 5 caused no increase over controls in ATPase-deficient foci, probably due to the lack of hepatocellular proliferation and the low rate of VC metabolism at this …

MaleCancer ResearchPathologymedicine.medical_specialtyVinyl CompoundsATPaseVinyl ChloridePartial hepatectomyBiologyVinyl chlorideAndrologychemistry.chemical_compoundLiver Neoplasms ExperimentalmedicineAnimalsBioassayCarcinogenAdenosine TriphosphatasesAge FactorsTransplacentalRats Inbred StrainsGeneral MedicineMetabolismRatsLiverchemistryRat liverbiology.proteinBiological AssayFemalePrecancerous ConditionsCarcinogenesis
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Clobetasol promotes neuromuscular plasticity in mice after motoneuronal loss via sonic hedgehog signaling, immunomodulation and metabolic rebalancing

2021

AbstractMotoneuronal loss is the main feature of amyotrophic lateral sclerosis, although pathogenesis is extremely complex involving both neural and muscle cells. In order to translationally engage the sonic hedgehog pathway, which is a promising target for neural regeneration, recent studies have reported on the neuroprotective effects of clobetasol, an FDA-approved glucocorticoid, able to activate this pathway via smoothened. Herein we sought to examine functional, cellular, and metabolic effects of clobetasol in a neurotoxic mouse model of spinal motoneuronal loss. We found that clobetasol reduces muscle denervation and motor impairments in part by restoring sonic hedgehog signaling and …

MaleCancer ResearchPhysiology129 StrainBiochemistryMiceDatabases GeneticMedicineMyocyteMotor NeuronsNeuronal PlasticitySkeletalSmoothened ReceptorHedgehog signaling pathwayMuscle atrophyMitochondriaAstrogliosisNeuroprotective AgentsMusclemedicine.symptomInflammation MediatorsSignal TransductionCholera ToxinMice 129 StrainhedgehogImmunologyMotor ActivityNeuroprotectionArticleDatabasesCellular and Molecular NeurosciencesmoothenedGeneticAnimalsHumansHedgehog ProteinsMuscle SkeletalHedgehogGlucocorticoidsMuscle DenervationQH573-671Animalbusiness.industryAmyotrophic Lateral SclerosisGlial biologyCell Biologymedicine.diseaseSaporinsSpineMitochondria MuscleDisease Models AnimalclobetasolinflammationCase-Control StudiesDisease ModelsDiseases of the nervous systemCytologySmoothenedbusinessEnergy MetabolismNeuroscienceOpen Field Test
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l-glutamine: a major substrate for tumor cells in vivo?

1987

From 65 human breast cancer xenografts investigated, a net glutamine uptake was found in 13 tumors (mean +/- SE: 15.7 +/- 4.5 nmol/g per min) whereas a net release (22.5 +/- 3.3 nmol/g per min) was observed in 40 tumors. In 12 tumors neither a significant net uptake nor a net release was obvious. There is experimental evidence that glutamine is taken up by cancer cells only at arterial concentrations greater than 0.5 mM. Another parameter determining glutamine utilization by tumor cells may be the tissue oxygenation. In hypoxic or anoxic tumor areas, glutamine oxidation is unlikely since oxygen is required for the reoxidation of coenzymes which are reduced in the course of this metabolic pa…

MaleCancer Researchmedicine.medical_specialtyGlutamineTransplantation HeterologousOxygenechemistry.chemical_elementBreast NeoplasmsBiologyModels BiologicalOxygenOxygen ConsumptionCarcinosarcomaIn vivoInternal medicinemedicineAnimalsHumanscomputer.programming_languageGlutaminolysisRats Inbred StrainsGeneral MedicineHydrogen-Ion ConcentrationTumor OxygenationRatsGlutamineTransplantationEndocrinologyOncologychemistryCancer cellFemaleEnergy MetabolismcomputerMathematicsNeoplasm TransplantationJournal of Cancer Research and Clinical Oncology
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Enzyme histochemical and immunohistochemical characterization of oval and parenchymal cells proliferating in livers of rats fed a choline-deficient/D…

1991

Male outbred Sprague-Dawley rats were fed a choline-deficient diet containing 0.10% DL-ethionine for up to 30 weeks. Liver slices from rats killed 4, 6, 10, 14, 22 and 30 weeks after starting the treatment were histochemically analyzed for the following parameters: basophilia, expression of cytokeratin 19 (which in the liver is bile duct epithelial cell-specific), glycogen content and activities of glycogen synthetase (SYN), glycogen phosphorylase (PHO), glucose-6-phosphatase (G6PASE), glucose-6-phosphate dehydrogenase (G6PDH), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), glycerin-3-phosphate dehydrogenase (G3PDH), 'malic enzyme' (MDH), alkaline phosphatase (ALKPASE) and gamma-glutamyl…

MaleCancer Researchmedicine.medical_specialtyPhosphorylasesPopulationGlycerolphosphate DehydrogenaseBiologyGlucosephosphate DehydrogenaseGlycogen phosphorylasechemistry.chemical_compoundMalate DehydrogenaseInternal medicineParenchymamedicineAnimalsEthionineeducationGlycogen synthaseeducation.field_of_studyEthionineGlycogenGlyceraldehyde-3-Phosphate DehydrogenasesRats Inbred StrainsGeneral Medicinegamma-GlutamyltransferaseAlkaline PhosphataseAnimal FeedImmunohistochemistryCholine DeficiencyLiver GlycogenRatsmedicine.anatomical_structureEndocrinologyGlycogen SynthasechemistryLiverHepatocyteFood Fortifiedbiology.proteinGlucose-6-PhosphataseAlkaline phosphataseKeratinsCell DivisionCarcinogenesis
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Induction of hepatic heme oxygenase-1 by diclofenac in rodents: role of oxidative stress and cytochrome P-450 activity

2003

Abstract Background/Aims : The role of oxidative stress in diclofenac hepatotoxicity is still not clear. This study examined whether the drug induced heme oxygenase-1 (HO-1), a stress protein. Methods : HO-1 mRNA and HO activity were measured in mouse liver and in rat hepatocytes after treatment with diclofenac parallel to release of serum alanine aminotransferase (ALT) and sorbitol dehydrogenase (SDH) as a marker of hepatic damage. Results : HO-1 was transcriptionally and dose-dependently induced by diclofenac in mouse liver and rat hepatocytes. HO-1 mRNA, ALT and SDH peaked at the same time. Mechanistic studies revealed that the drug synergized with buthionine sulfoximine (BSO) in lowerin…

MaleCarcinoma HepatocellularDiclofenacCytochromeMice Inbred StrainsOxidative phosphorylationPharmacologymedicine.disease_causeMicechemistry.chemical_compoundCytochrome P-450 Enzyme SystemCell Line TumormedicineAnimalsCytochrome P-450 Enzyme InhibitorsHumansButhionine sulfoximineEnzyme InhibitorsButhionine SulfoximineDose-Response Relationship DrugHepatologybiologyLiver NeoplasmsMembrane ProteinsCytochrome P450GlutathioneAcetylcysteineRatsHeme oxygenaseOxidative Stressstomatognathic diseasesmedicine.anatomical_structureLiverchemistryBiochemistryEnzyme InductionHepatocyteHeme Oxygenase (Decyclizing)Hepatocytesbiology.proteinFemaleHeme Oxygenase-1Oxidative stressJournal of Hepatology
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Effect of metal ion catalyzed oxidation of rifamycin SV on cell viability and metabolic performance of isolated rat hepatocytes.

1991

The effect of rifamycin SV on metabolic performance and cell viability was studied using isolated hepatocytes from fed, starved and glutathione (GSH) depleted rats. The relationships between GSH depletion, nutritional status of the cells, glucose metabolism, lactate dehydrogenase (LDH) leakage and malondialdehyde (MDA) production in the presence of rifamycin SV and transition metal ions was investigated. Glucose metabolism was impaired in isolated hepatocytes from both fed and starved animals, the effect is dependent on the rifamycin SV concentration and is enhanced by copper (II). Oxygen consumption by isolated hepatocytes from starved rats was also increased by copper (II) and a partial i…

MaleCell SurvivalIronLipid peroxidationchemistry.chemical_compoundOxygen ConsumptionLactate dehydrogenaseMalondialdehydemedicineAnimalsViability assayMolecular BiologybiologyL-Lactate DehydrogenaseChemistryGluconeogenesisRats Inbred StrainsCell BiologyGlutathioneMetabolismCatalaseThiobarbituratesGlutathioneRifamycinsRatsmedicine.anatomical_structureGluconeogenesisBiochemistryLiverCatalaseHepatocytebiology.proteinLipid PeroxidationOxidation-ReductionCopperBiochimica et biophysica acta
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