Search results for "DNA Breaks"

showing 7 items of 37 documents

Immediate biomarker responses to benzo[a]pyrene in polluted and unpolluted populations of the blue mussel (Mytilus edulis L.) at high-latitudes.

2008

Immediate biomarker responses of two high-latitude populations of the blue mussel Mytilus edulis to benzo[a]pyrene (B[a]P) were evaluated. Mussels collected from a clean and a polluted site in southwest Iceland were exposed to the nominal dose of 100 μg B[a]P L−l for 3 h, after 4 days of acclimatization in clean seawater. To test the sensitivity to the toxicant and immediate biological responses, the following biomarkers were used: DNA single strand breaks, heart rate and feeding rate.All the biomarkers revealed differences between the study sites. Irrespective of the origin of the organisms, the short time exposure to the high B[a]P concentration did not induce DNA single strand breaks or …

Settore BIO/07 - EcologiaTime FactorsMytilus edulisIcelandZoologyAcclimatizationToxicologychemistry.chemical_compoundSensitivityHeart RateBenzo(a)pyreneEcotoxicologyAnimalsDNA Breaks Single-Strandedlcsh:Environmental sciencesGeneral Environmental Sciencelcsh:GE1-350biologyBiomarkerFeeding BehaviorBivalviabiology.organism_classificationAdaptation PhysiologicalMytilusBenzo[a]pyrenechemistryBenzo(a)pyreneBenzopyreneGenotoxicityFeeding rateMytilus eduliBlue musselBiomarkersToxicantEnvironment international
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Complete-active-space second-order perturbation theory (CASPT2//CASSCF) study of the dissociative electron attachment in canonical DNA nucleobases ca…

2015

Low-energy (0-3 eV) ballistic electrons originated during the irradiation of biological material can interact with DNA/RNA nucleobases yielding transient-anion species which undergo decompositions. Since the discovery that these reactions can eventually lead to strand breaking of the DNA chains, great efforts have been dedicated to their study. The main fragmentation at the 0-3 eV energy range is the ejection of a hydrogen atom from the specific nitrogen positions. In the present study, the methodological approach introduced in a previous work on uracil [I. González-Ramírez et al., J. Chem. Theory Comput. 8, 2769-2776 (2012)] is employed to study the DNA canonical nucleobases fragmentations…

Valence (chemistry)GuaninePyrimidineGuanineAdenineDNA BreaksGeneral Physics and AstronomyElectronsHydrogen atomDNAMolecular physicsIonNucleobaseThyminechemistry.chemical_compoundCytosinechemistryThermodynamicsComplete active spacePhysical and Theoretical ChemistryAtomic physicsUracilThymineHydrogenThe Journal of chemical physics
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WRN protects against topo I but not topo II inhibitors by preventing DNA break formation

2008

The Werner syndrome helicase/3′-exonuclease (WRN) is a major component of the DNA repair and replication machinery. To analyze whether WRN is involved in the repair of topoisomerase-induced DNA damage we utilized U2-OS cells, in which WRN is stably down-regulated (wrn-kd), and the corresponding wild-type cells (wrn-wt). We show that cells not expressing WRN are hypersensitive to the toxic effect of the topoisomerase I inhibitor topotecan, but not to the topoisomerase II inhibitor etoposide. This was shown by mass survival assays, colony formation and induction of apoptosis. Upon topotecan treatment WRN deficient cells showed enhanced DNA replication inhibition and S-phase arrest, whereas af…

congenital hereditary and neonatal diseases and abnormalitiesWerner Syndrome HelicaseDNA RepairCell SurvivalDNA damageDNA repairBlotting WesternApoptosisBone NeoplasmsBiologyTopoisomerase-I InhibitorBiochemistryArticleWerner Syndrome HelicaseColony-Forming Units AssayHistonesTumor Cells CulturedmedicineHumansTopoisomerase II InhibitorsEnzyme InhibitorsRNA Small InterferingeducationMolecular BiologyEtoposideOsteosarcomaeducation.field_of_studyRecQ HelicasesTopoisomeraseCell CycleDNA Breaksnutritional and metabolic diseasesCell BiologyAntineoplastic Agents PhytogenicMolecular biologyDNA Topoisomerases Type IIExodeoxyribonucleasesBromodeoxyuridineDNA Topoisomerases Type IDNA Replication InhibitionCancer researchbiology.proteinTopoisomerase I InhibitorsTopoisomerase-II InhibitorTopotecanCamptothecinmedicine.drugDNA Repair
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Single- and Double-Strand Breaks of Dry DNA Exposed to Protons at Bragg-Peak Energies

2017

International audience; Ultrathin layers (<20 nm) of pBR322 plasmid DNA were deposited onto 2.5 μm thick polyester films and exposed to proton Bragg-peak energies (90–3000 keV) at various fluences. A quantitative analysis of radio-induced DNA damage is reported here in terms of single- and double-strand breaks (SSB and DSB, respectively). The corresponding yields as well as G-values and the cross sections exhibit fairly good agreement with the rare available data, stemming from close experimental conditions, namely, based on α particle irradiation. SSB/DSB rates appear to be linear when plotted against linear energy transfer (LET) in the whole energy range studied. All the data present a ma…

cross-sectionProtonPolyestersLinear energy transferBragg peak7. Clean energyclustered DNA damage030218 nuclear medicine & medical imagingdamage yield03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFragmentation (mass spectrometry)Materials ChemistryDNA Breaks Double-StrandedLinear Energy TransferDNA Breaks Single-StrandedIrradiationPhysical and Theoretical Chemistryradiochemical yieldDouble strandRange (particle radiation)DNASurfaces Coatings and Films[ PHYS.PHYS.PHYS-CHEM-PH ] Physics [physics]/Physics [physics]/Chemical Physics [physics.chem-ph]chemistry030220 oncology & carcinogenesis[PHYS.PHYS.PHYS-CHEM-PH]Physics [physics]/Physics [physics]/Chemical Physics [physics.chem-ph]ProtonsAtomic physicsDNAPlasmidsBragg-Peaksingle and double strand breakThe Journal of Physical Chemistry B
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Targeting DNA double strand break repair with hyperthermia and DNA-PKcs inhibition to enhance the effect of radiation treatment

2016

// Bregje van Oorschot 1 , Giovanna Granata 1 , Simone Di Franco 2 , Rosemarie ten Cate 1 , Hans M. Rodermond 1 , Matilde Todaro 3 , Jan Paul Medema 1 , Nicolaas A.P. Franken 1 1 Laboratory for Experimental Oncology and Radiobiology (LEXOR), Center for Experimental Molecular Medicine, Department of Radiation Oncology, Academic Medical Center, Cancer Genomics Center, Amsterdam, The Netherlands 2 Department of Surgical, Oncological and Stomatological Sciences (DICHIRONS), Cellular and Molecular Pathophysiology Laboratory, University of Palermo, Palermo, Italy 3 Biomedical Department of Internal and Specialistic Medicine (DIBIMIS), University of Palermo, Palermo, Italy Correspondence to: Nicol…

double-strand break0301 basic medicineRadiation-Sensitizing AgentsPathologymedicine.medical_specialtyDNA End-Joining RepairRadiobiologyDNA repairDNA damageMorpholinesmedicine.medical_treatmentMice NudeUterine Cervical NeoplasmsDNA repairBreast NeoplasmsDNA-Activated Protein KinaseRadiation ToleranceMice03 medical and health sciences0302 clinical medicineCancer stem cellTumor Cells CulturedAnimalsHumansMedicineDNA Breaks Double-StrandedHomologous RecombinationDNA-PKcsdouble-strand breaksRadiotherapybusiness.industryCancerradiation oncologyHyperthermia Inducedhyperthermiamedicine.diseaseRadiation therapyradiation oncology.030104 developmental biologyOncologyChromones030220 oncology & carcinogenesisCancer cellNeoplastic Stem CellsCancer researchFemalebusinessResearch PaperDNA DamageOncotarget
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Inhibition of Rac1 signaling by lovastatin protects against anthracycline-induced cardiac toxicity

2011

Normal tissue damage limits the efficacy of anticancer therapy. For anthracyclines, the clinically most relevant adverse effect is cardiotoxicity. The mechanisms involved are poorly understood and putative cardioprotectants are controversially discussed. Here, we show that the lipid-lowering drug lovastatin protects rat H9c2 cardiomyoblasts from doxorubicin in vitro. Protection by lovastatin is related to inhibition of the Ras-homologous GTPase Rac1. It rests on a reduced formation of DNA double-strand breaks, resulting from the inhibition of topoisomerase II by doxorubicin. Doxorubicin transport and reactive oxygen species are not involved. Protection by lovastatin was confirmed in vivo. I…

rac1 GTP-Binding ProteinCancer ResearchAnthracyclineDoxorubicin transportCardiac fibrosismedicine.medical_treatmentImmunologyPharmacologyBiologyDNA damage responsestatinsMiceCellular and Molecular NeuroscienceRho GTPasespolycyclic compoundsmedicineAnimalsDNA Breaks Double-StrandedMyocytes CardiacDoxorubicinLovastatinanthracyclinesCardiotoxicityAntibiotics AntineoplasticTroponin IConnective Tissue Growth FactorCell Biologymedicine.diseaseRatsCTGFDNA Topoisomerases Type IICytokinenormal tissue damageDoxorubicinOriginal Articlelipids (amino acids peptides and proteins)LovastatinAtrial Natriuretic FactorSignal Transductionmedicine.drugCell Death &amp; Disease
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Late Activation of Stress-activated Protein Kinases/c-Jun N-terminal Kinases Triggered by Cisplatin-induced DNA Damage in Repair-defective Cells

2011

Although stress-activated protein kinases/c-Jun N-terminal kinases (SAPK/JNK) are rapidly activated by genotoxins, the role of DNA damage in this response is not well defined. Here we show that the SEK1/MKK4-mediated dual phosphorylation of SAPK/JNK (Thr-183/Tyr-185) correlates with the level of cisplatin-DNA adducts at late times (16–24 h) after drug treatment in both human and mouse cells. Transfection of platinated plasmid DNA also caused SAPK/JNK activation. A defect in transcription-coupled nucleotide excision repair resting on a mutation in Cockayne syndrome group B protein promoted the late SAPK/JNK activation following cisplatin exposure. Signaling to SAPK/JNK was accompanied by act…

rho GTP-Binding ProteinsDNA RepairMAP Kinase Kinase 4DNA repairDNA damageDNA damage response; DNA repair; cisplatin-DNA adducts; SAPK/JNKp38 mitogen-activated protein kinasesAntineoplastic AgentsCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesDNA and ChromosomesBiologyBiochemistryAtaxia Telangiectasia Mutated ProteinsDNA AdductsMiceRadiation IonizingAnimalsHumansDNA Breaks Double-StrandedMolecular BiologyReplication protein ACells CulturedMice KnockoutKinaseTumor Suppressor ProteinsJNK Mitogen-Activated Protein KinasesCell BiologyMolecular biologyDNA-Binding ProteinsEnzyme Activationc-Jun N-terminal kinasesbiology.proteinCisplatinSignal TransductionNucleotide excision repairJournal of Biological Chemistry
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