Search results for "Quinolizines"

showing 7 items of 7 documents

Overexpression of Ogg1 in mammalian cells: effects on induced and spontaneous oxidative DNA damage and mutagenesis

1999

Chinese hamster ovary cell lines (AA8 and AS52) were stably transfected to overexpress hOgg1 protein, the human DNA repair glycosylase for 7,8-dihydro-8-oxoguanine (8-oxoG). In the transfectants, the repair rate of 8-oxoG residues induced by either potassium bromate or the photosensitizer [R]-1-[(10-chloro-4-oxo-3-phenyl-4H-benzo[a]quinolizin-1-yl)-carbo nyl ]-2-pyrrolidinemethanolplus light was up to 3-fold more rapid than in the parental cells. However, the improved repair had little effect on the mutagenicity of potassium bromate in the guanine phosphoribosyl transferase (gpt) locus of the OGG1-transfected AS52 cells. The steady-state (background) levels of DNA base modifications sensiti…

Cancer ResearchPyrrolidinesDNA RepairPhotochemistryDNA repairDNA damageBiologyTransfectionPolymerase Chain ReactionCell LineDNA-formamidopyrimidine glycosylasechemistry.chemical_compoundCricetulusGenes ReporterCricetinaeAnimalsheterocyclic compoundsN-Glycosyl HydrolasesPhotosensitizing AgentsBromatesChinese hamster ovary cellOvaryGeneral MedicineTransfectionDNA repair protein XRCC4OxidantsMolecular biologyOxidative StressDNA-Formamidopyrimidine GlycosylasechemistryGenes BacterialMutagenesisDNA glycosylaseEnzyme InductionFemaleQuinolizinesDNADNA DamageCarcinogenesis
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Rapid inactivation and proteasome-mediated degradation of OGG1 contribute to the synergistic effect of hyperthermia on genotoxic treatments

2013

Inhibition of DNA repair has been proposed as a mechanism underlying heat-induced sensitization of tumour cells to some anticancer treatments. Base excision repair (BER) constitutes the main pathway for the repair of DNA lesions induced by oxidizing or alkylating agents. Here, we report that mild hyperthermia, without toxic consequences per se, affects cellular DNA glycosylase activities, thus impairing BER. Exposure of cells to mild hyperthermia leads to a rapid and selective inactivation of OGG1 (8-oxoguanine DNA glycosylase) associated with the relocalisation of the protein into a detergent-resistant cellular fraction. Following its inactivation, OGG1 is ubiquitinated and directed to pro…

HyperthermiaProteasome Endopeptidase ComplexPyrrolidinesDNA RepairDNA repairUbiquitin-Protein Ligases[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]BiochemistryDNA Glycosylases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineUbiquitinEnzyme StabilitymedicineHumans[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Molecular BiologyComputingMilieux_MISCELLANEOUSCell Proliferation030304 developmental biologyCell Nucleus0303 health sciencesPhotosensitizing AgentsbiologyCell growthUbiquitinationCell BiologyBase excision repairmedicine.diseaseMolecular biology[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Protein TransportProteasomechemistryDNA glycosylase030220 oncology & carcinogenesisProteolysisCancer researchbiology.proteinHeat-Shock ResponseQuinolizinesDNADNA DamageHeLa Cells
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Erratum to: Cetuximab-induced skin exanthema: prophylactic and reactive skin therapy are equally effective

2013

Purpose Treatment with cetuximab is accompanied by the development of an acneiform follicular skin exanthema in more than 80 % of patients. Severe exanthema (grade III/IV) develops in about 9–19 % of patients with the necessity of cetuximab dose reduction or cessation. Methods The study presented was a retrospective analysis of 50 gastrointestinal cancer patients treated with cetuximab in combination with either FOLFIRI or FOLFOX. One cohort of 15 patients received an in-house reactive skin protocol upon development of an exanthema. A second cohort of 15 patients received a skin prophylaxis starting with the first dose of cetuximab before clinical signs of toxicity. A third historic group o…

MaleCancer ResearchColorectal cancerAdministration TopicalAdministration OralCetuximabMinocyclineGastroenterologyPeritoneal NeoplasmPeritoneal NeoplasmsGastrointestinal NeoplasmsSkinHematologyintegumentary systemCetuximabTherapy reactiveMultimodal therapyVitamin K 1General MedicineMiddle AgedCombined Modality TherapyAnti-Bacterial AgentsSurvival RateTreatment OutcomeAppendiceal NeoplasmsOncologyColonic NeoplasmsAdenocarcinomaFemaleErratumQuinolizinesFluoroquinolonesmedicine.drugmedicine.medical_specialtyPrednisoloneEGFRDetergentsAntineoplastic AgentsAdenocarcinomaAntibodies Monoclonal HumanizedDisease-Free SurvivalMetronidazoleRashInternal medicineIntestinal NeoplasmsmedicineCombined Modality TherapyHumansSurvival rateAgedRetrospective StudiesOriginal PaperRectal Neoplasmsbusiness.industryRetrospective cohort studyAntibiotic ProphylaxisExanthemamedicine.diseaseDermatologydigestive system diseasesSurgerybusinessJournal of Cancer Research and Clinical Oncology
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Pharmacokinetics, bioavailability and absorption of flumequine in the rat.

1999

Abstract The study demonstrates that the oral extent of bioavailability of flumequine in the rat, relative to the intravenous injection, is complete (0.94±0.04) and not significantly different from that found by the intraduodenal route (0.95±0.04). The rate of oral bioavailability, however, is slow ( k a =1.20±0.07 h −1 ; T max =2.0 h), but enough to maintain plasma levels above the minimal inhibitory concentration of the most common pathogens for an extended period of time (about 10 h). The reason for the oral absorption slowness could be a slow gastric emptying, an adsorption to the gastric mucosae, a precipitation in the gastric medium or any other feature concerning the stomach as the i…

MaleDuodenumPharmaceutical ScienceAdministration OralBiological AvailabilityPharmacologyModels BiologicalRandom AllocationPharmacokineticsAnti-Infective AgentsOral administrationEnterohepatic CirculationmedicineAnimalsRats WistarEnterohepatic circulationAntibacterial agentGastric emptyingChemistryStomachGeneral MedicineBioavailabilityRatsmedicine.anatomical_structureIntestinal AbsorptionFlumequineQuinolizinesBiotechnologymedicine.drugFluoroquinolonesEuropean journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V
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Synthesis of alkaloids by Stevens rearrangement of nitrile-stabilized ammonium ylides: (±)-laudanosine, (±)-laudanidine, (±)-armepavine, (±)-7-methox…

2013

The Stevens rearrangement of nitrile-stabilized ammonium ylides in conjunction with the reductive removal of the nitrile function permits the facile construction of α-branched amines from α-aminonitriles. We employed this reaction sequence for the preparation of (±)-laudanosine, (±)-laudanidine and (±)-armepavine, (±)-7-methoxycryptopleurine, and (±)-xylopinine from two closely related and readily accessible bicyclic α-aminonitriles. The final products were obtained in high to almost quantitative yields (71–98%) from the quaternary ammonium salts obtained by N-alkylation of these starting materials.

NitrileBicyclic moleculeMolecular StructureArmepavineOrganic ChemistryBerberine AlkaloidsStereoisomerismIsoquinolinesBenzylisoquinolinesLaudanosineQuaternary Ammonium Compoundschemistry.chemical_compoundchemistryStevens rearrangement7-methoxycryptopleurineNitrilesXylopinineOrganic chemistryAmmoniumQuinolizinesThe Journal of organic chemistry
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Oxidative DNA damage and mutations induced by a polar photosensitizer, Ro19-8022.

1999

The oxidative DNA damage induced by the polar photosensitizer Ro19-8022 in the presence of light was studied and correlated with the associated mutagenicity. Both in isolated DNA and AS52 Chinese hamster ovary cells, photoexcited Ro19-8022 gave rise to a DNA damage profile that was similar to that caused by singlet oxygen: base modifications sensitive to the repair endonuclease Fpg protein, which according to high-performance liquid chromatography (HPLC) analysis were predominantly 8-hydroxyguanine (8-oxoG) residues, were generated in much higher yield than single-strand breaks, sites of base loss (AP sites) and oxidative pyrimidine modifications sensitive to endonuclease III. Fifty percent…

PyrrolidinesDNA damageMolecular Sequence DataCHO CellsBiologyToxicologymedicine.disease_causechemistry.chemical_compoundPlasmidCricetinaeGeneticsmedicineAnimalsPhotosensitizerMutation frequencyMolecular BiologyGenePhotosensitizing AgentsBase SequenceCell-Free SystemChinese hamster ovary cellOxidative StressBiochemistrychemistryDNA ViralMutationDNAOxidative stressQuinolizinesDNA DamageMutation research
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Is the repair of oxidative DNA base modifications inducible by a preceding DNA damage induction?

2007

In mammalian cells, 7,8-dihydro-8-oxoguanine (8-oxoG) and some other oxidative guanine modifications are removed from the DNA by base excision repair, which is initiated by OGG1 protein. We have tested whether this repair is inducible in mouse embryonic fibroblasts (MEFs), MCF-7 breast cancer cells and primary human fibroblasts by a pretreatment with the photosensitizer Ro19-8022 plus light, which generates predominantly 8-oxoG, or with methyl methanesulfonate (MMS), which generates alkylated bases and abasic sites (AP sites). The results indicate that the repair rate of the oxidative guanine modifications induced by the photosensitizer was not increased if a priming dose of the oxidative o…

PyrrolidinesTime FactorsDNA RepairDNA repairGuanineDNA damageBiologymedicine.disease_causeBiochemistryMicechemistry.chemical_compoundTumor Cells CulturedmedicineAnimalsHumansheterocyclic compoundsAntineoplastic Agents AlkylatingBase PairingMolecular BiologyPhotosensitizing AgentsGuanosineDNACell BiologyBase excision repairGlutathioneFibroblastsMethyl MethanesulfonateGlutathioneMolecular biologyMethyl methanesulfonateOxidative StresschemistryFemaleOxidation-ReductionQuinolizinesDNAOxidative stressDNA DamageDNA Repair
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