Search results for "DNA Damage"

showing 10 items of 534 documents

Exposure to environmental radionuclides is associated with altered metabolic and immunity pathways in a wild rodent

2019

Wildlife inhabiting environments contaminated by radionuclides face putative detrimental effects of exposure to ionizing radiation, with biomarkers such as an increase in DNA damage and/or oxidative stress commonly associated with radiation exposure. To examine the effects of exposure to radiation on gene expression in wildlife, we conducted a de novo RNA sequencing study of liver and spleen tissues from a rodent, the bank vole Myodes glareolus. Bank voles were collected from the Chernobyl Exclusion Zone (CEZ), where animals were exposed to elevated levels of radionuclides, and from uncontaminated areas near Kyiv, Ukraine. Counter to expectations, we did not observe a strong DNA damage resp…

0106 biological sciences0301 basic medicineRodentDNA Repairmedicine.disease_cause01 natural sciencessäteilybiologiachemistry.chemical_compoundRadiation IonizingMyodes glareolusstable isotopepollutionaineenvaihduntaBeta oxidationradionuclides2. Zero hungerbiologyArvicolinaeFatty AcidsRadiation ExposureRNAseqBank voleMolecular AdaptationLiverimmuunijärjestelmäOriginal ArticleUkraineOxidation-ReductionmetsämyyräDNA damageDNA repair010603 evolutionary biologyMicrobiology03 medical and health sciencesImmunitybiology.animalGeneticsmedicineAnimalsEcology Evolution Behavior and SystematicsRadioisotopesFatty acid metabolismLipid metabolismDNAbiology.organism_classificationLipid MetabolismOxidative Stress030104 developmental biologychemistryChernobyl Nuclear Accident13. Climate actionImmune SystemRNAORIGINAL ARTICLESOxidative stressSpleenDNA DamageMutagens
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Environmental aircraft noise aggravates oxidative DNA damage, granulocyte oxidative burst and nitrate resistance inOgg1–/–mice

2020

Background: Large epidemiological studies point towards a link between the incidence of arterial hypertension, ischaemic heart disease, metabolic disease and exposure to traffic noise, supporting t...

0301 basic medicine030102 biochemistry & molecular biologybusiness.industryEnvironmental stressorTraffic noiseGeneral MedicineGranulocytemedicine.diseasemedicine.disease_causeBiochemistryRespiratory burstOxidative dna damage03 medical and health scienceschemistry.chemical_compound030104 developmental biologymedicine.anatomical_structureNitratechemistryImmunologymedicineEndothelial dysfunctionbusinessOxidative stressFree Radical Research
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Investigation of Isoindolo[2,1-a] quinoxaline-6-imines as Topoisomerase I Inhibitors with Molecular Modeling Methods

2017

Background: Isoindolo[2,1-alpha] quinoxalines constitute an important class of compounds which demonstrated potent antiproliferative activity against different human tumor cell lines and topoisomerase I inhibitors. In particular, their water soluble imine or iminium salts recently synthesized showed potent growth inhibitory effect on NCI-60 tumor cell line panel and biological studies performed on the most active compounds demonstrated that they cause DNA damage via topoisomerase I poisoning. Objective: Herein, we investigate with molecular modeling methods, the common features responsible for topoisomerase I inhibition of the water-soluble isoindolo[2,1-alpha] quinoxalin-6-imines, by compa…

0301 basic medicine030103 biophysicsMolecular modelStereochemistryDNA damageAntineoplastic AgentsIsoindolesTopoisomerase-I InhibitorCrystallography X-RayaromatechinStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compoundQuinoxalinetopotecanantiproliferativeCell Line TumorNeoplasmsQuinoxalinesquinoxalineDrug DiscoveryHumansCell Proliferationbiologypharmacophore modelTopoisomeraseIminiumGeneral MedicineSettore CHIM/08 - Chimica FarmaceuticaMolecular Docking SimulationTopoisomerase IindenoisoquinolineDNA Topoisomerases Type IchemistryDocking (molecular)dockingbiology.proteinMolecular MedicineTopoisomerase I; quinoxaline; antiproliferative; topotecan; aromatechin; indenoisoquinoline; docking; pharmacophore modelIminesTopoisomerase I InhibitorsPharmacophore
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Repurposing of Bromocriptine for Cancer Therapy

2018

Bromocriptine is an ergot alkaloid and dopamine D2 receptor agonist used to treat Parkinson’s disease, acromegaly, hyperprolactinemia, and galactorrhea, and more recently diabetes mellitus. The drug is also active against pituitary hormone-dependent tumors (prolactinomas and growth-hormone producing adenomas). We investigated, whether bromocriptine also inhibits hormone-independent and multidrug-resistant (MDR) tumors. We found that bromocriptine was cytotoxic towards drug-sensitive CCRF-CEM, multidrug-resistant CEM/ADR5000 leukemic cells as well as wild-type or multidrug-resistant ABCB5-transfected HEK293 cell lines, but not sensitive or BCRP-transfected multidrug-resistant MDA-MB-231 brea…

0301 basic medicineAbcg2DNA damageDNA repairCellneoplasmsergot alkaloids03 medical and health sciencesDopamine receptor D2AcromegalymedicinePharmacology (medical)Original ResearchbromocriptinepharmacogenomicsPharmacologydrug repurposingbiologybusiness.industrylcsh:RM1-950medicine.diseaseBromocriptinelcsh:Therapeutics. Pharmacology030104 developmental biologymedicine.anatomical_structureMitochondrial respiratory chainCancer researchbiology.proteinbusinessmedicine.drugFrontiers in Pharmacology
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Acute telomerase components depletion triggers oxidative stress as an early event previous to telomeric shortening

2018

Loss of function of dyskerin (DKC1), NOP10 and TIN2 are responsible for different inheritance patterns of Dyskeratosis congenita (DC; ORPHA1775). They are key components of telomerase (DKC1 and NOP10) and shelterin (TIN2), and play an important role in telomere homeostasis. They participate in several fundamental cellular processes by contributing to Dyskeratosis congenita through mechanisms that are not fully understood. Presence of oxidative stress was postulated to result from telomerase ablation. However, the resulting disturbed redox status can promote telomere attrition by generating a vicious circle, which promotes cellular senescence. This fact prompted us to study if acute loss of …

0301 basic medicineAgingTelomeraseTelomere-Binding ProteinsClinical BiochemistryCell Cycle ProteinsBiologymedicine.disease_causeBiochemistryDyskeratosis CongenitaDyskerin03 medical and health sciencesTelomere HomeostasisRibonucleoproteins Small NucleolarmedicineHumanslcsh:QH301-705.5TelomeraseCellular SenescenceTelomere ShorteningRibonucleoproteinlcsh:R5-920TelomeropathiesOrganic ChemistryNuclear ProteinsShelterinmedicine.diseaseMolecular biologyTelomereCell biologyOxidative Stress030104 developmental biologylcsh:Biology (General)DNA damageRNA InterferenceAntioxidantlcsh:Medicine (General)Oxidative stressDyskeratosis congenitaResearch PaperHeLa CellsRedox Biology
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Cytotoxic effects of zearalenone and its metabolites and antioxidant cell defense in CHO-K1 cells.

2016

Zearalenone (ZEA) and its metabolites (α-zearalenol; α-ZOL, β-zearalenol; β-ZOL) are secondary metabolites of Fusarium fungi that produce cell injury. The present study explores mycotoxin-induced cell damage and cellular protection mechanisms in CHO-K1 cells. Cytotoxicity has been determined by reactive oxygen species (ROS) production and DNA damage. ROS production was determined using the fluorescein assay and DNA strand breakage by comet assay. Intracellular protection systems were glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD). The results demonstrated that all mycotoxins increased the ROS levels up to 5.3-fold the control levels in CHO-K1 …

0301 basic medicineAntioxidantDNA damagemedicine.medical_treatmentImmunoblottingCHO CellsToxicologyAntioxidantsSuperoxide dismutase03 medical and health scienceschemistry.chemical_compoundCricetulusCricetinaemedicineAnimalsEstrogens Non-SteroidalCell damagechemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasebiologySuperoxide DismutaseGlutathione peroxidasefood and beveragesGeneral MedicineGlutathionemedicine.diseaseCatalaseGlutathioneComet assay030104 developmental biologychemistryBiochemistrybiology.proteinZearalenoneZeranolComet AssayReactive Oxygen SpeciesOxidation-ReductionFood ScienceDNA DamageFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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In vitro mechanisms of Beauvericin toxicity: A review.

2017

Beauvericin (BEA) is a mycotoxin produced by many species of fungus Fusarium and by Beauveria bassiana; BEA is a natural contaminant of cereals and cereals based products and possesses a wide variety of biological properties. The mechanism of action seems to be related to its ionophoric activity, that increases ion permeability in biological membranes. As a consequence, BEA causes cytotoxicity in several cell lines and is capable to produce oxidative stress at molecular level. Moreover, BEA is genotoxic (produces DNA fragmentation, chromosomal aberrations and micronucleus) and causes apoptosis with the involvement of mitochondrial pathway. However, several antioxidant mechanisms protect cel…

0301 basic medicineAntioxidantmedicine.medical_treatmentApoptosisToxicologymedicine.disease_cause03 medical and health scienceschemistry.chemical_compound0404 agricultural biotechnologyFusariumDepsipeptidesmedicineAnimalsHumansCytotoxicityMycotoxin04 agricultural and veterinary sciencesGeneral MedicineMycotoxins040401 food scienceBeauvericinOxidative Stress030104 developmental biologychemistryBiochemistryToxicityDNA fragmentationMicronucleusOxidative stressFood ScienceDNA DamageFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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Theabrownin triggersDNAdamage to suppress human osteosarcoma U2OScells by activating p53 signalling pathway

2018

Abstract Osteosarcoma becomes the second leading cause of cancer death in the younger population. Current outcomes of chemotherapy on osteosarcoma were unsatisfactory to date, demanding development of effective therapies. Tea is a commonly used beverage beneficial to human health. As a major component of tea, theabrownin has been reported to possess anti‐cancer activity. To evaluate its anti‐osteosarcoma effect, we established a xenograft model of zebrafish and employed U2OS cells for in vivo and in vitro assays. The animal data showed that TB significantly inhibited the tumour growth with stronger effect than that of chemotherapy. The cellular data confirmed that TB‐triggered DNA damage an…

0301 basic medicineApoptosisCatechinHistones0302 clinical medicineRNA Small InterferingZebrafisheducation.field_of_studyCaspase 3ChemistryCell CycleGene Expression Regulation NeoplasticLarva030220 oncology & carcinogenesisMolecular MedicineOsteosarcomaOriginal ArticlePoly(ADP-ribose) PolymerasesSignal TransductionCell SurvivalDNA damagePoly ADP ribose polymerasePopulationBone NeoplasmsCaspase 303 medical and health sciencesAnimal dataosteosarcomaCell Line TumormedicineAnimalsHumanstheabrownineducationP53OsteoblastsMesenchymal Stem CellsOriginal ArticlesCell Biologymedicine.diseaseAntineoplastic Agents PhytogenicXenograft Model Antitumor AssaysKi-67 Antigen030104 developmental biologyApoptosisCell cultureCancer researchDNA damageCisplatinTumor Suppressor Protein p53Journal of Cellular and Molecular Medicine
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Oleocanthal exerts antitumor effects on human liver and colon cancer cells through ROS generation

2017

The beneficial health properties of the Mediterranean diet are well recognized. The principle source of fat in Mediterranean diet is extra-virgin olive oil (EVOO). Oleocanthal (OC) is a naturally occurring minor phenolic compound isolated from EVOO, which has shown a potent anti-inflammatory activity, by means of its ability to inhibit the cyclooxygenase (COX) enzymes COX-1 and COX-2. A large body of evidence indicates that phenols exhibit anticancer activities. The aim of the present study was to evaluate the potential anticancer effects of OC in hepatocellular carcinoma (HCC) and colorectal carcinoma (CRC) models. A panel of human HCC (HepG2, Huh7, Hep3B and PLC/PRF/5) and CRC (HT29, SW48…

0301 basic medicineCancer ResearchCarcinoma HepatocellularHepatocellular carcinomaOleocanthalExtra-virgin olive oilCellApoptosisCyclopentane Monoterpenes03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhenolsOleocanthalmedicineHumansCyclooxygenase InhibitorsViability assayOlive OilCaspaseCell ProliferationAldehydesbiologyCell growthLiver NeoplasmsApoptosiHep G2 CellsCell cycledigestive system diseasesColorectal carcinoma030104 developmental biologymedicine.anatomical_structureOncologychemistryApoptosisCell culture030220 oncology & carcinogenesisImmunologybiology.proteinCancer researchReactive oxygen specieColorectal NeoplasmsReactive Oxygen SpeciesDNA DamageInternational Journal of Oncology
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Knockdown of hnRNPK leads to increased DNA damage after irradiation and reduces survival of tumor cells.

2017

Radiotherapy is an important treatment option in the therapy of multiple tumor entities among them head and neck squamous cell carcinoma (HNSCC). However, the success of radiotherapy is limited by the development of radiation resistances. Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is a cofactor of p53 and represents a potential target for radio sensitization of tumor cells. In this study, we analyzed the impact of hnRNPK on the DNA damage response after gamma irradiation. By yH2AX foci analysis, we found that hnRNPK knockdown increases DNA damage levels in irradiated cells. Tumor cells bearing a p53 mutation showed increased damage levels and delayed repair. Knockdown of hnRNPK appl…

0301 basic medicineCancer ResearchDNA damageCell Survivalmedicine.medical_treatmentmedicine.disease_causeRadiation ToleranceHeterogeneous-Nuclear Ribonucleoprotein KHistones03 medical and health sciences0302 clinical medicineCell Line TumormedicineCarcinomaGene Knockdown TechniquesHumansMutationGene knockdownChemistrySquamous Cell Carcinoma of Head and NeckStem CellsGeneral Medicinemedicine.diseaseHead and neck squamous-cell carcinomaRadiation therapy030104 developmental biologyCell cultureHead and Neck Neoplasms030220 oncology & carcinogenesisGene Knockdown TechniquesCancer researchCarcinoma Squamous CellTumor Suppressor Protein p53DNA DamageCarcinogenesis
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