Search results for "Dative"

showing 10 items of 2381 documents

In human retinoblastoma Y79 cells okadaic acid-parthenolide co-treatment induces synergistic apoptotic effects, with PTEN as a key player.

2013

Retinoblastoma is the most common intraocular malignancy of childhood. In developing countries, treatment is limited, long-term survival rates are low and current chemotherapy causes significant morbidity to pediatric patients and significantly limits dosing. Therefore there is an urgent need to identify new therapeutic strategies to improve the clinical outcome of patients with retinoblastoma. here, we investigated the effects of two natural compounds okadaic acid (OKa) and parthenolide (PN) on human retinoblastoma Y79 cells. For the first time we showed that OKa/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-akt levels, increasin…

Cancer ResearchCell SurvivalGene ExpressionAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundSettore BIO/10 - BiochimicaCell Line TumorOkadaic AcidmedicinePTENCytotoxic T cellHumansParthenolideViability assayProtein kinase BCell ShapePharmacologyRetinoblastomaPTEN PhosphohydrolaseRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2Okadaic acidmedicine.diseaseGlutathioneOxidative StressOncologychemistryApoptosisCancer researchbiology.proteinMolecular Medicineretinoblastoma Y79 cells synergistic apoptotic effects oxidative stress natural drugs PTEN/Akt/Mdm2/p53 pathway parthenolide okadaic acid.Drug Screening Assays AntitumorTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktSesquiterpenesResearch PaperCancer biologytherapy
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Influence of nitric oxide on the generation and repair of oxidative DNA damage in mammalian cells

2002

We have analysed the effects of endogenously and exogenously generated nitric oxide (NO) in cultured mammalian fibroblasts on: (i) the steady-state (background) levels of oxidative DNA base modifications; (ii) the susceptibility of the cells to the induction of additional DNA damage and micronuclei by H(2)O(2); and (iii) the repair kinetics of various types of DNA modifications. Steady-state levels of oxidative DNA base modifications, measured by means of an alkaline elution assay in combination with the repair endonuclease Fpg protein, were similar in NO-overproducing B6 mouse fibroblasts stably transfected with an inducible NO synthase (iNOS) and in control cells. Increased oxidative dama…

Cancer ResearchDNA RepairDNA damageDNA repairNitric Oxide Synthase Type IIMutagenAlkenesBiologyNitric OxideTransfectionmedicine.disease_causeMicechemistry.chemical_compoundmedicineAnimalsNitric Oxide DonorsDose-Response Relationship DrugHydrogen PeroxideGeneral MedicineTransfectionFibroblastsCell biologyBiochemistrychemistryNitric Oxide SynthaseDNAGenotoxicityPeroxynitriteOxidative stressDNA DamageCarcinogenesis
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Spontaneous mutagenesis in Csb(m/m)Ogg1⁻(/)⁻ mice is attenuated by dietary resveratrol.

2010

Oxidative DNA modifications such as 7,8-dihydro-8-oxoguanine (8-oxoG) are generated endogenously in apparently all living cells. The defect of the repair of 8-oxoG in Csb m/m Ogg1 ―/― mice results in elevated basal levels of these lesions and increased frequencies of spontaneous mutations, which initiate tumorigenesis in the liver if cell proliferation is stimulated. Here, we describe that the phytoalexin resveratrol, applied either for 7 days per gavage (100 mg/kg body wt) or for 3―9 months in the diet (0.04% ad libitum), reduces the endogenous oxidative DNA base damage in the livers of the Csb m/m Ogg1 ―/― mice by 20―30% (P < 0.01). A small but consistent effect is also observed in the wi…

Cancer ResearchDNA damageSOD1SOD2Gene ExpressionMice TransgenicBiologyResveratrolSuperoxide dismutasechemistry.chemical_compoundMiceStilbenesAnimalschemistry.chemical_classificationReverse Transcriptase Polymerase Chain ReactionGlutathione peroxidaseMutagenesisAntimutagenic AgentsGeneral MedicineMolecular biologyDietOxidative StressCell killingchemistryBiochemistryLiverMutagenesisResveratrolbiology.proteinDNA DamageCarcinogenesis
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The Peroxisome Proliferator WY-14,643 Promotes Hepatocarcinogenesis Caused by Endogenously Generated Oxidative DNA Base Modifications in Repair-Defic…

2007

Abstract Basal levels of endogenously generated oxidative DNA modifications such as 7,8-dihydro-8-oxoguanine (8-oxoG) are present in apparently all mammalian cells, but their relevance for the generation of spontaneous cancers remains to be established. Both the 8-oxoG levels and the resulting spontaneous mutations are increased in the livers of Csbm/m/Ogg1−/− mice, which are deficient in the repair of 8-oxoG. In order to determine the consequences of these additional oxidative DNA modifications and mutations and thus assess the tumor initiating potency of this type of endogenous DNA damage, we treated Csbm/m/Ogg1−/− mice and repair-proficient controls with the peroxisome proliferator WY-14…

Cancer ResearchGuanineDNA RepairRatónDNA damageEndogenyOxidative phosphorylationBiologymedicine.disease_causeDNA GlycosylasesMicechemistry.chemical_compoundLiver Neoplasms ExperimentalmedicineAnimalsPoly-ADP-Ribose Binding ProteinsCocarcinogenesisCell growthLiver cellMolecular biologyMice Inbred C57BLOxidative StressDNA Repair EnzymesPyrimidinesLiverOncologyBiochemistrychemistryMutationPeroxisome ProliferatorsCarcinogenesisPrecancerous ConditionsDNADNA DamageCancer Research
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Influence of glutathione levels and heat-shock on the steady-state levels of oxidative DNA base modifications in mammalian cells

1999

The effects of thiols, ascorbic acid and thermal stress on the basal (steady-state) levels of oxidative DNA base modifications were studied. In various types of untreated cultured mammalian cells, the levels of total glutathione were found to be inversely correlated with the levels of DNA base modifications sensitive to the repair endonuclease Fpg protein, which include 8-hydroxyguanine (8-oxoG). A depletion of glutathione by treatment with buthionine sulphoximine increased the steady-state level in AS52 Chinese hamster cells by approximately 50%. However, additional thiols in the culture medium did not reduce the level of Fpg-sensitive base modifications: 0-10 mM N-acetylcysteine had no ef…

Cancer ResearchHot TemperatureDNA damageGlutathione reductaseOxidative phosphorylationmedicine.disease_causeCell LineMicechemistry.chemical_compoundHsp27CricetinaeTumor Cells CulturedmedicineAnimalsHumansEnzyme InhibitorsButhionine SulfoximineN-Glycosyl HydrolasesHeat-Shock ProteinsbiologyChemistryGeneral MedicineGlutathioneAscorbic acidGlutathioneOxidative StressDNA-Formamidopyrimidine GlycosylaseBiochemistrybiology.proteinOxidative stressDNA DamageHeLa CellsCysteineCarcinogenesis
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Autophagy and mitochondrial alterations in human retinal pigment epithelial cells induced by ethanol: implications of 4-hydroxy-nonenal

2014

Retinal pigment epithelium has a crucial role in the physiology and pathophysiology of the retina due to its location and metabolism. Oxidative damage has been demonstrated as a pathogenic mechanism in several retinal diseases, and reactive oxygen species are certainly important by-products of ethanol (EtOH) metabolism. Autophagy has been shown to exert a protective effect in different cellular and animal models. Thus, in our model, EtOH treatment increases autophagy flux, in a concentration-dependent manner. Mitochondrial morphology seems to be clearly altered under EtOH exposure, leading to an apparent increase in mitochondrial fission. An increase in 2′,7′-dichlorofluorescein fluorescenc…

Cancer ResearchImmunologyApoptosisRetinal Pigment EpitheliumMitochondrionBiologymedicine.disease_causeCell LineLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundRetinal DiseasesmedicineAutophagyHumanschemistry.chemical_classificationReactive oxygen speciesAldehydesRetinal pigment epitheliumEthanolAutophagyRetinalEpithelial CellsCell BiologyCell biologyMitochondriaOxidative Stressmedicine.anatomical_structurechemistryBiochemistryMitochondrial fissionOriginal ArticleReactive Oxygen SpeciesOxidative stressCell Death & Disease
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Breast cancer stem cells rely on fermentative glycolysis and are sensitive to 2-deoxyglucose treatment

2014

A number of studies suggest that cancer stem cells are essential for tumour growth, and failure to target these cells can result in tumour relapse. As this population of cells has been shown to be resistant to radiation and chemotherapy, it is essential to understand their biology and identify new therapeutic approaches. Targeting cancer metabolism is a potential alternative strategy to counteract tumour growth and recurrence. Here we applied a proteomic and targeted metabolomic analysis in order to point out the main metabolic differences between breast cancer cells grown as spheres and thus enriched in cancer stem cells were compared with the same cells grown in adherent differentiating c…

Cancer ResearchImmunologyPopulationPyruvate KinaseBreast NeoplasmsOxidative phosphorylationBiologyDeoxyglucoseOxidative PhosphorylationCellular and Molecular Neurosciencechemistry.chemical_compoundPYRUVATE-KINASE M2Cancer stem cellLactate dehydrogenaseCell Line TumorHumansGlycolysiseducationSettore BIO/10 - BIOCHIMICASettore MED/04 - Patologia Generaleeducation.field_of_studyL-Lactate DehydrogenaseCell growthTUMOR-GROWTHSettore BIO/12Cell BiologyCell biologychemistry2-deoxyglucose BCSCNeoplastic Stem CellsFemaleOriginal ArticleStem cellGlycolysisPyruvate kinase
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PO-002 Angiotensin II-induced hypertension increases the mutation frequency in the rat kidney

2018

Introduction Epidemiological studies revealed an increased risk for kidney cancer in hypertensive patients. In many of these patients, the blood pressure regulating renin angiotensin aldosterone system (RAAS) is activated. A stimulated RAAS can lead to oxidative stress and DNA damage, as we have shown both in vitro and in animal models of hypertension. Here, we used a rat model to quantify mutations generated by 20 weeks of angiotensin II-infusion. Material and methods BigBlue+/- rats, which carry a transgenic lacI gene for mutation analysis, were treated with 0.4 mg angiotensin II/kg/day with the help of osmotic minipumps. Urinary samples were collected in week 15 by placing the rats into …

Cancer ResearchKidneymedicine.medical_specialtyDNA damagebusiness.industryUrinary systemmedicine.disease_causeAngiotensin IImedicine.anatomical_structureEndocrinologyOncologyInternal medicineRenal physiologyRenin–angiotensin systemmedicineMutation frequencybusinessOxidative stressESMO Open
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Artesunate induces oxidative DNA damage, sustained DNA double-strand breaks, and the ATM/ATR damage response in cancer cells.

2011

Abstract Artesunate, the active agent from Artemisia annua L. used in the traditional Chinese medicine, is being applied as a first-line drug for malaria treatment, and trials are ongoing that include this drug in cancer therapy. Despite increasing interest in its therapeutic application, the mode of cell killing provoked by artesunate in human cells is unknown. Here, we show that artesunate is a powerful inducer of oxidative DNA damage, giving rise to formamidopyrimidine DNA glycosylase–sensitive sites and the formation of 8-oxoguanine and 1,N6-ethenoadenine. Oxidative DNA damage was induced in LN-229 human glioblastoma cells dose dependently and was paralleled by cell death executed by ap…

Cancer ResearchProgrammed cell deathDNA RepairRAD51Drug Evaluation PreclinicalArtesunateApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiologyProtein Serine-Threonine KinasesModels Biologicalchemistry.chemical_compoundNeoplasmsTumor Cells CulturedHumansDNA Breaks Double-StrandedTumor Suppressor ProteinsMolecular biologyAntineoplastic Agents PhytogenicArtemisininsUp-RegulationNon-homologous end joiningDNA-Binding ProteinsOxidative StressCell killingOncologychemistryArtesunateApoptosisCancer cellHomologous recombinationDNA DamageMolecular cancer therapeutics
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The plasma membrane channel ORAI1 mediates detrimental calcium influx caused by endogenous oxidative stress.

2013

The mouse hippocampal cell line HT22 is an excellent model for studying the consequences of endogenous oxidative stress. Addition of extracellular glutamate depletes the cells of glutathione (GSH) by blocking the glutamate-cystine antiporter system x(c)(-). GSH is the main antioxidant in neurons and its depletion induces a well-defined program of cell death called oxytosis, which is probably synonymous with the iron-dependent form of non-apoptotic cell death termed ferroptosis. Oxytosis is characterized by an increase of reactive oxygen species and a strong calcium influx preceding cell death. We found a significant reduction in store-operated calcium entry (SOCE) in glutamate-resistant HT2…

Cancer ResearchProgrammed cell deathORAI1 ProteinSTIM1AntiporterImmunologychemistry.chemical_elementApoptosisCalciumBiologymedicine.disease_causeAntioxidantsCell LineCellular and Molecular Neurosciencechemistry.chemical_compoundMicemedicineAnimalsStromal Interaction Molecule 1RNA Small InterferingStromal Interaction Molecule 2Calcium metabolismMembrane GlycoproteinsORAI1Cell MembraneCell BiologySTIM2GlutathioneGlutathioneCell biologyOxidative StresschemistryCalciumOriginal ArticleCalcium ChannelsReactive Oxygen SpeciesOxidative stressSOCECell deathdisease
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