Search results for " STRESS"

showing 10 items of 3936 documents

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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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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WIN induces apoptotic cell death in human colon cancer cells through a block of autophagic flux dependent on PPARγ down-regulation.

2014

Cannabinoids have been reported to possess anti-tumorigenic activity in cancer models although their mechanism of action is not well understood. Here, we show that the synthetic cannabinoid WIN55,212-2 (WIN)-induced apoptosis in colon cancer cell lines is accompanied by endoplasmic reticulum stress induction. The formation of acidic vacuoles and the increase in LC3-II protein indicated the involvement of autophagic process which seemed to play a pro-survival role against the cytotoxic effects of the drug. However, the enhanced lysosomal membrane permeabilization (LMP) blocked the autophagic flux after the formation of autophagosomes as demonstrated by the accumulation of p62 and LC3, two ma…

Cancer ResearchMorpholinesClinical BiochemistryPharmaceutical ScienceDown-RegulationAntineoplastic AgentsApoptosisBiologyNaphthalenesDownregulation and upregulationSettore BIO/10 - BiochimicaCell Line TumormedicineAutophagyGene silencingHumansViability assayPharmacologyEndoplasmic reticulumBiochemistry (medical)AutophagyCannabinoids PPARγ ER stress autophagy/apoptosis interplay colon carcinoma cellsCell BiologyEndoplasmic Reticulum StressCell biologyBenzoxazinesMitochondriaPPAR gammaMechanism of actionApoptosisColonic NeoplasmsUnfolded protein responsemedicine.symptomSignal TransductionApoptosis : an international journal on programmed cell death
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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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The role of oxidative stress in apoptosis induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid in human colon adenocarcinoma …

2008

Histone deacetylase inhibitors (HDACIs) activate genes that promote cell cycle arrest and apoptosis in a number of tumor cells. This study showed that suberoylanilide hydroxamic acid (SAHA), a potent and commonly used HDACI, induced apoptosis in human colon adenocarcinoma HT-29 cells in a time- and dose-dependent manner. This effect was accompanied by the induction of oxidative stress, dissipation of mitochondrial transmembrane potential and activation of executioner caspases. Moreover, SAHA increased the levels of phosphorylated active forms of p38 and JNK. The addition of either the antioxidant N-acetylcysteine or the specific inhibitor of NADPH oxidase diphenylene iodonium chloride reduc…

Cancer ResearchProgrammed cell deathmedicine.drug_classCell Survivalp38 mitogen-activated protein kinasesBlotting WesternApoptosisAdenocarcinomamedicine.disease_causeHydroxamic AcidsAntioxidantsSettore BIO/10 - BiochimicamedicineHumansEnzyme InhibitorsProtein kinase BCaspaseMembrane Potential MitochondrialVorinostatbiologyHistone deacetylase inhibitorEnzyme ActivationHistone Deacetylase InhibitorsOxidative StressOncologyBiochemistryApoptosisCaspasesColonic NeoplasmsCancer researchbiology.proteinHistone deacetylaseReactive Oxygen Speciescolon adenomacarcinoma cells histone deacetylase inhibitors apoptosisHT29 CellsOxidative stressSignal TransductionInternational journal of oncology
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Wavelength dependence of oxidative DNA damage induced by UV and visible light.

1997

DNA damage induced by UV radiation and visible light (290-500 nm) in AS52 Chinese hamster cells was analysed by an alkaline elution assay with specific repair endonucleases. Cells were exposed to extensively filtered monochrome or broad-band radiation. Between 290 and 315 nm, the ratio of base modifications sensitive to Fpg protein (i.e. 8-hydroxyguanine and formamidopyrimidines) and T4 endonuclease V (i.e. cyclobutane pyrimidine dimers) was constant (approximately 1:200), indicating that the direct excitation of DNA is responsible for both types of damage in this range of the spectrum. While the yield of pyrimidine dimers per unit dose continued to decrease exponentially beyond 315 nm, the…

Cancer ResearchPyrimidinebiologyLightSinglet oxygenDNA damageUltraviolet RaysPyrimidine dimerDose-Response Relationship RadiationGeneral MedicineCHO CellsPhotochemistrymedicine.disease_causechemistry.chemical_compoundEndonucleaseOxidative StresschemistryCricetinaebiology.proteinmedicineAnimalsDNAOxidative stressVisible spectrumDNA DamageCarcinogenesis
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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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The p53 Tumor Suppressor Network Is a Key Responder to Microenvironmental Components of Chronic Inflammatory Stress

2005

Abstract Activation of the p53 network plays a central role in the inflammatory stress response associated with ulcerative colitis and may modulate cancer risk in patients afflicted with this chronic disease. Here, we describe the gene expression profiles associated with four microenvironmental components of the inflammatory response (NO•, H2O2, DNA replication arrest, and hypoxia) that result in p53 stabilization and activation. Isogenic HCT116 and HCT116 TP53−/− colon cancer cells were exposed to the NO• donor Sper/NO, H2O2, hypoxia, or hydroxyurea, and their mRNA was analyzed using oligonucleotide microarrays. Overall, 1,396 genes changed in a p53-dependent manner (P < 0.001), wit…

Cancer ResearchTumor suppressor geneColorectal cancerInflammationBiologymedicine.disease_causeArticleGene expressionmedicineHumansNitric Oxide DonorsInflammationReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell CycleHydrogen PeroxideCell cycleHypoxia (medical)Flow CytometryHCT116 Cellsmedicine.diseaseCell HypoxiaGene expression profilingOxidative StressOncologyImmunologyNitrogen OxidesSpermineTumor Suppressor Protein p53medicine.symptomOxidative stressCancer Research
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Sexual, bladder and bowel function following different minimally invasive techniques of radical hysterectomy in patients with early-stage cervical ca…

2021

Abstract Purpose Despite the establishment of radical surgery for therapy of cervical cancer, data on quality of life and patient-reported outcomes are scarce. The aim of this retrospective cohort study was to evaluate bladder, bowel and sexual function in women who underwent minimally invasive surgery for early-stage cervical cancer. Methods From 2007–2013, 261 women underwent laparoscopically assisted radical vaginal hysterectomy (LARVH = 45), vaginally assisted laparoscopic or robotic radical hysterectomy (VALRRH = 61) or laparoscopic total mesometrial resection (TMMR = 25) and 131 of them completed the validated German version of the Australian Pelvic Floor Questionnaire (PFQ). Results …

Cancer ResearchUrinary Incontinence StressUrinary incontinenceUterine Cervical NeoplasmsUrinary incontinence0302 clinical medicinePostoperative ComplicationsRobotic Surgical ProceduresSurveys and QuestionnairesHysterectomy VaginalPostoperative PeriodCervical cancerIntestinal Disease030219 obstetrics & reproductive medicinePelvic floorUrinary Bladder DiseasesGeneral MedicineOrgan SizeMiddle Agedmedicine.anatomical_structureDyspareuniaOncology030220 oncology & carcinogenesisVaginaVaginaFemalemedicine.symptomResearch ArticleQuality of lifeAdultmedicine.medical_specialtySexual functionHysterectomy03 medical and health sciencesPelvic floor dysfunctionMinimally invasive surgerymedicineHumansPatient Reported Outcome MeasuresRadical surgeryRadical HysterectomyPelvic floor functionAgedNeoplasm StagingRetrospective Studies...business.industryUrinary Bladder Overactivemedicine.diseaseSurgeryIntestinal DiseasesSexual Dysfunction PhysiologicalCase-Control StudiesCervical cancerLaparoscopyPostoperative ComplicationSexual functionbusinessConstipationClinical & Translational Oncology
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