Search results for "DNA Damage"

showing 10 items of 534 documents

Apoptosis induced by MNNG in human TK6 lymphoblastoid cells is p53 and Fas/CD95/Apo-1 related.

2003

Agents inducing O(6)-methylguanine (O(6)MeG) in DNA, such as N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), are not only highly mutagenic and carcinogenic but also cytotoxic because of the induction of apoptosis. In CHO fibroblasts, apoptosis triggered by O(6)MeG requires cell proliferation and MutSalpha-dependent mismatch repair and is related to the induction of DNA double-strand breaks (DSBs). Furthermore, it is mediated by Bcl-2 degradation and does not require p53 for which the cells were mutated [Cancer Res. 60 (2000) 5815]. Here we studied cytotoxicity and apoptosis induced by MNNG in a pair of human lymphoblastoid cells expressing wild-type p53 (TK6) and mutant p53 (WTK1) and show tha…

MethylnitronitrosoguanidineCell SurvivalHealth Toxicology and MutagenesisApoptosisCHO CellsBiologyCell LineBcl-2-associated X proteinCricetinaeProto-Oncogene ProteinsGeneticsCytotoxic T cellAnimalsHumansfas Receptorbcl-2-Associated X ProteinMitogen-Activated Protein Kinase 1Cell growthLymphoblastFas receptorMolecular biologyKineticsCell killingProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisbiology.proteinTumor Suppressor Protein p53DNA DamageMutation research
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Iron regulatory mechanisms in Saccharomyces cerevisiae

2020

Iron is an essential micronutrient for all eukaryotic organisms because it participates as a redox cofactor in many cellular processes. However, excess iron can damage cells since it promotes the generation of reactive oxygen species. The budding yeast Saccharomyces cerevisiae has been used as a model organism to study the adaptation of eukaryotic cells to changes in iron availability. Upon iron deficiency, yeast utilizes two transcription factors, Aft1 and Aft2, to activate the expression of a set of genes known as the iron regulon, which are implicated in iron uptake, recycling and mobilization. Moreover, Aft1 and Aft2 activate the expression of Cth2, an mRNA-binding protein that limits t…

Microbiology (medical)DNA damageSaccharomyces cerevisiaelcsh:QR1-502Saccharomyces cerevisiaeMicroorganismesyeastMicrobiologylcsh:Microbiology03 medical and health sciencesTranscriptional regulationiron deficiencyFongsiron metabolismPost-transcriptional regulationTranscription factorGene030304 developmental biology0303 health sciencesbiology030306 microbiologyChemistryPost-transcriptional regulationiron excessbiology.organism_classificationYeastCell biologyCytosolReguloniron homeostasisFerro
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ALS monocyte-derived microglia reveal cytoplasmic TDP-43 accumulation, DNA damage, and cell-specific impairment of phagocytosis associated with disea…

2020

AbstractAimsAmyotrophic lateral sclerosis (ALS) is a multifactorial neurodegenerative disease characterised by the loss of upper and lower motor neurons. Neuroinflammation mediated by microglial activation is evident in post-mortem brain tissues, and in brain imaging of patients with ALS. However, the exact role of microglia in ALS remains to be elucidated partly due to the lack of an accurate microglial model system that is able to recapitulate the clinical pathology of ALS. Moreover, direct sampling of microglia from patients with ALS is not feasible, further limiting the study of microglial function in ALS. To address this shortcoming, we describe an approach that generates monocyte-deri…

Microgliabusiness.industryDNA damagePhagocytosisDiseaseHuman brainmedicine.diseasemedicine.anatomical_structureImmunologymedicineAmyotrophic lateral sclerosisbusinessPathologicalNeuroinflammation
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Mitochondria as sources and targets of damage in cellular aging.

2011

Mitochondria are considered as the most important cellular sources and targets of free radicals. They are also a source of signalling molecules that regulate cell cycle, proliferation, and apoptosis. Denham Harman postulated the free radical theory of aging in 1956. Previously Rebecca Gershman showed that radiation toxicity could be attributed to free radical damage. Subsequently, Jaime Miquel formulated the mitochondrial free radical theory of aging. We have shown that mitochondrial size, membrane potential, inner membrane mass and peroxide production is altered inside cells in old animals. These result in an increase in the oxidative damage to mitochondrial DNA with aging that can be prev…

Mitochondrial DNAFree RadicalsDNA damageBiochemistry (medical)Clinical BiochemistryGeneral MedicineMitochondrionBiologyMitochondrial Sizemedicine.disease_causeAntioxidantsCell biologyMitochondriaOxidative StressMitochondrial biogenesisApoptosismedicineAnimalsHumansOxidative stressCellular SenescenceFree-radical theory of agingDNA DamageClinical chemistry and laboratory medicine
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New Insights Into Mitochondrial DNA Reconstruction and Variant Detection in Ancient Samples

2021

Ancient DNA (aDNA) studies are frequently focused on the analysis of the mitochondrial DNA (mtDNA), which is much more abundant than the nuclear genome, hence can be better retrieved from ancient remains. However, postmortem DNA damage and contamination make the data analysis difficult because of DNA fragmentation and nucleotide alterations. In this regard, the assessment of the heteroplasmic fraction in ancient mtDNA has always been considered an unachievable goal due to the complexity in distinguishing true endogenous variants from artifacts. We implemented and applied a computational pipeline for mtDNA analysis to a dataset of 30 ancient human samples from an Iron Age necropolis in Poliz…

Mitochondrial DNANuclear genelcsh:QH426-470DNA damagemitochondrial DNAComputational biologySettore BIO/08 - AntropologiaBiologyGenomeHeteroplasmyHaplogrouplcsh:Geneticsancient DNA mitochondrial DNA NUMTs heteroplasmy variant detection anthropologyAncient DNAancient DNA; heteroplasmy; mitochondrial DNA; NUMTs; variant detectionGeneticsMolecular MedicineDNA fragmentationheteroplasmyancient DNANUMTsvariant detectionGenetics (clinical)Original ResearchFrontiers in Genetics
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Reactive oxygen species derived from the mitochondrial respiratory chain are not responsible for the basal levels of oxidative base modifications obs…

2004

The mitochondrial electron transport chain (ETC) is the most important source of reactive oxygen species (ROS) in mammalian cells. To assess its relevance to the endogenous generation of oxidative DNA damage in the nucleus, we have compared the background (steady-state) levels of oxidative DNA base modifications sensitive to the repair glycosylase Fpg (mostly 7,8-dihydro-8-oxoguanine) in wild-type HeLa cells and HeLa rho0 cells. The latter are depleted of mitochondrial DNA and therefore are unable to produce ROS in the ETC. Although the levels of ROS measured by flow cytometry and redox-sensitive probes in rho0 cells were only 10-15% those of wild-type cells, steady-state levels of oxidativ…

Mitochondrial ROSCarbonyl Cyanide m-Chlorophenyl HydrazoneMitochondrial DNADNA damageCells[SDV]Life Sciences [q-bio]Oxidative phosphorylationMitochondrionBiologyBiochemistryElectron Transport03 medical and health sciences0302 clinical medicinePhysiology (medical)AnimalsHumansComputingMilieux_MISCELLANEOUS030304 developmental biologyCell Nucleus0303 health sciencesGuanosineNucleotidesEscherichia coli ProteinsDNAFlow CytometryMitochondriaNuclear DNAMitochondrial respiratory chainDNA-Formamidopyrimidine GlycosylaseBiochemistryDNA glycosylaseMacrolidesReactive Oxygen SpeciesOxidation-Reduction030217 neurology & neurosurgeryDNA DamageHeLa Cells
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Manganese superoxide dismutase and aldehyde dehydrogenase deficiency increase mitochondrial oxidative stress and aggravate age-dependent vascular dys…

2008

AimsImbalance between pro- and antioxidant species (e.g. during aging) plays a crucial role for vascular function and is associated with oxidative gene regulation and modification. Vascular aging is associated with progressive deterioration of vascular homeostasis leading to reduced relaxation, hypertrophy, and a higher risk of thrombotic events. These effects can be explained by a reduction in free bioavailable nitric oxide that is inactivated by an age-dependent increase in superoxide formation. In the present study, mitochondria as a source of reactive oxygen species (ROS) and the contribution of manganese superoxide dismutase (MnSOD, SOD-2) and aldehyde dehydrogenase (ALDH-2) were inves…

Mitochondrial ROSMaleAgingPhysiologyVasodilator AgentsMitochondrionVascular dysfunctionmedicine.disease_causeMitochondria HeartMuscle Smooth Vascularchemistry.chemical_compoundMiceEndothelial dysfunctionAortachemistry.chemical_classificationMice KnockoutbiologySuperoxideAldehyde Dehydrogenase MitochondrialAge FactorsVasodilationBiochemistryCardiology and Cardiovascular MedicineMitochondrial aldehyde dehydrogenasemedicine.medical_specialty8-oxodGOxidative phosphorylationDNA MitochondrialSuperoxide dismutaseManganese superoxide dismutaseddc:570Physiology (medical)Internal medicinemedicineAnimalsReactive oxygen speciesDose-Response Relationship DrugSuperoxide DismutaseMitochondrial oxidative stressOriginal ArticlesAldehyde Dehydrogenasemedicine.diseaseMice Inbred C57BLOxidative StressEndocrinologychemistrybiology.proteinEndothelium VascularReactive Oxygen SpeciesOxidative stressDNA DamageCardiovascular research
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Mitochondrial Oxidative Stress, Mitochondrial DNA Damage and Their Role in Age-Related Vascular Dysfunction

2015

The prevalence of cardiovascular diseases is significantly increased in the older population. Risk factors and predictors of future cardiovascular events such as hypertension, atherosclerosis, or diabetes are observed with higher frequency in elderly individuals. A major determinant of vascular aging is endothelial dysfunction, characterized by impaired endothelium-dependent signaling processes. Increased production of reactive oxygen species (ROS) leads to oxidative stress, loss of nitric oxide (•NO) signaling, loss of endothelial barrier function and infiltration of leukocytes to the vascular wall, explaining the low-grade inflammation characteristic for the aged vasculature. We here disc…

Mitochondrial ROSmedicine.medical_specialtyMitochondrial DNADNA RepairInflammationReviewBiologyMitochondrionmedicine.disease_causeDNA MitochondrialCatalysisAntioxidantsNitric oxideInorganic Chemistrylcsh:Chemistrychemistry.chemical_compoundInternal medicinemedicineAnimalsHumansPhysical and Theoretical ChemistryEndothelial dysfunctionMolecular Biologylcsh:QH301-705.5Spectroscopychemistry.chemical_classificationReactive oxygen speciesmitochondrial oxidative stressOrganic Chemistryagingmitochondrial DNA damageGeneral Medicinevascular dysfunctionmedicine.diseaseComputer Science ApplicationsMitochondriaOxidative StressEndocrinologyBiochemistrychemistrylcsh:Biology (General)lcsh:QD1-999Cardiovascular Diseasesmedicine.symptomReactive Oxygen SpeciesOxidative stressDNA DamageInternational Journal of Molecular Sciences
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The Impact of CdS Nanoparticles on Ploidy and DNA Damage of Rucola (Eruca sativa Mill.) Plants

2015

The genotoxic effect of cadmium sulfide nanoparticles (CdS NPs) of different sizes in rucola (Eruca sativaMill.) plants was assessed. It was confirmed that nanoparticles < 5 nm in size were more toxic than larger particles at an identical mass concentration. Significant differences in cell ploidy, as well as in the mitotic index, were detected between control and treated samples. Differences in the DNA banding pattern between control samples and samples after treatment with cadmium sulfide nanoparticles were significant and detected at different places as the appearance or elimination of DNA fragments. Fluorescence images showed that cadmium sulfide nanoparticles smaller than 5 nm in siz…

Mitotic indexMaterials scienceArticle SubjectbiologyDNA damageNanoparticlefood and beveragesErucabiology.organism_classificationCadmium sulfidechemistry.chemical_compoundMembranechemistryBotanylcsh:Technology (General)lcsh:T1-995General Materials SciencePloidyDNANuclear chemistryJournal of Nanomaterials
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In Silico Insights into the SARS CoV-2 Main Protease Suggest NADH Endogenous Defences in the Control of the Pandemic Coronavirus Infection

2020

COVID-19 is a pandemic health emergency faced by the entire world. The clinical treatment of the severe acute respiratory syndrome (SARS) CoV-2 is currently based on the experimental administration of HIV antiviral drugs, such as lopinavir, ritonavir, and remdesivir (a nucleotide analogue used for Ebola infection). This work proposes a repurposing process using a database containing approximately 8000 known drugs in synergy structure- and ligand-based studies by means of the molecular docking and descriptor-based protocol. The proposed in silico findings identified new potential SARS CoV-2 main protease (MPRO) inhibitors that fit in the catalytic binding site of SARS CoV-2 MPRO. Several sel…

Models Molecular0301 basic medicineAgingmedicine.medical_treatmentcoronaviruslcsh:QR1-502Viral Nonstructural Proteinsmedicine.disease_causelcsh:Microbiology0302 clinical medicineSettore BIO/10 - BiochimicaCoronavirus 3C ProteasesCoronavirusvirus diseasesLopinavirHypothesisMolecular Docking SimulationCysteine EndopeptidasesDrug repositioningInfectious Diseases030220 oncology & carcinogenesisCoronavirus InfectionsOxidation-Reductionmedicine.drugDNA damageIn silicoPneumonia ViralBiologyAntiviral AgentsHIV-proteaseBetacoronavirus03 medical and health sciencesSARS-CoV-2 main proteaseVirologymedicineHumansComputer SimulationProtease InhibitorsPandemicsBinding SitesProteaseSARS-CoV-2Drug RepositioningCOVID-19HIV Protease InhibitorsDRUDIT web servicemolecular dockingNADbiology.organism_classificationVirologySettore CHIM/08 - Chimica FarmaceuticaCOVID-19 Drug Treatmentcoronaviru030104 developmental biologyNADHRitonavirBetacoronavirusDNA Damage
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