Search results for "DNA Damage"

showing 10 items of 534 documents

Different patterns of in vivo pro-oxidant states in a set of cancer- or aging-related genetic diseases

2008

A comparative evaluation is reported of pro-oxidant states in 82 patients with ataxia telangectasia (AT), Bloom syndrome (BS), Down syndrome (DS), Fanconi anemia (FA), Werner syndrome (WS), and xeroderma pigmentosum (XP) vs 98 control donors. These disorders display cancer proneness, and/or early aging, and/or other clinical features. The measured analytes were: (a) leukocyte and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), (b) blood glutathione (GSSG and GSH), (c) plasma glyoxal (Glx) and methylglyoxal (MGlx), and (d) some plasma antioxidants [uric acid (UA) and ascorbic acid (AA)]. Leukocyte 8-OHdG levels ranked as follows: WS>BS approximately FA approximately XP>DS approximately AT appr…

AdultMalemedicine.medical_specialtyDown syndromeXeroderma pigmentosumAdolescentmedicine.disease_causeBiochemistrychemistry.chemical_compoundAtaxia TelangiectasiaPhysiology (medical)Internal medicinemedicineHumansBloom syndromeChildAgedXeroderma PigmentosumMethylglyoxalDeoxyguanosineGlutathioneGlyoxalMiddle AgedAscorbic acidmedicine.diseasePyruvaldehydeGlutathioneEndocrinologyFanconi AnemiaantioxidantschemistryBiochemistry8-Hydroxy-2'-DeoxyguanosineUric acidOxidative streFemaleWerner SyndromeDown SyndromeReactive Oxygen SpeciesOxidative stressBloom SyndromeDNA Damage
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The smokeless tobacco habit and DNA damage: A systematic review and meta-analysis.

2018

Background The aim of this systematic review was to evaluate the frequency of micronuclei or other DNA damage in the oral mucosa of adults that have smokeless tobacco habits compared to adults that not have these habits. Material and Methods We searched PubMed, Scopus, Web of Science, LILACS, BBO and Cochrane Library and SIGLE. We also surveyed gray literature. We included only clinical trials that compare the frequency of micronuclei or other DNA damage in the oral mucosa of adults that have smokeless tobacco habits compared to adults that not have these habits. Quality assessments of the selected trials were evaluated by two independent reviewers, using the Effective Public Health Practic…

Adultmedicine.medical_specialtyTobacco SmokelessDatabases FactualMEDLINEletterReviewCochrane LibraryHabits03 medical and health sciences0302 clinical medicineInternal medicineTobaccomedicineHumansGeneral DentistryMicronucleus TestsOral Medicine and Pathologybusiness.industrySmokingMouth Mucosa030206 dentistry:CIENCIAS MÉDICAS [UNESCO]Confidence intervalClinical trialOtorhinolaryngologySmokeless tobaccoStrictly standardized mean differenceMeta-analysisMicronucleus testUNESCO::CIENCIAS MÉDICASMouth NeoplasmsSurgeryPublic HealthbusinessDNA DamageMedicina oral, patologia oral y cirugia bucal
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In vitro and in vivo evaluation of AFB1 and OTA-toxicity through immunofluorescence and flow cytometry techniques: A systematic review

2022

Due to the globalization, mycotoxins have been considered a major risk to human health being the main con- taminants of foodstuffs. Among them, AFB1 and OTA are the most toxic and studied. Therefore, the goal of this review is to deepen the knowledge about the toxicological effects that AFB1 and OTA can induce on human health by using flow cytometry and immunofluorescence techniques in vitro and in vivo models. The examination of the selected reports shows that the majority of them are focused on immunotoxicity while the rest are con- cerned about nephrotoxicity, hepatotoxicity, gastrointestinal toxicity, neurotoxicity, embryotoxicity, reproduc- tive system, breast, esophageal and lung toxi…

Aflatoxin B1Fluorescent Antibody TechniqueAliments ToxicologiaApoptosisGeneral MedicineFlow CytometryToxicologySalut públicaOchratoxinsOxidative StressAliments ContaminacióAnimalsHumansSalutDNA DamageFood ScienceFood and Chemical Toxicology
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Repair of oxidatively generated DNA damage in Cockayne syndrome

2013

Defects in the repair of endogenously (especially oxidatively) generated DNA modifications and the resulting genetic instability can potentially explain the clinical symptoms of Cockayne syndrome (CS), a hereditary disease characterized by developmental defects and neurological degeneration. In this review, we describe the evidence for the involvement of CSA and CSB proteins, which are mutated in most of the CS patients, in the repair and processing of DNA damage induced by reactive oxygen species and the implications for the induction of cell death and mutations. Taken together, the data demonstrate that CSA and CSB, in addition to their established role in transcription-coupled nucleotide…

AgingDNA RepairTranscription GeneticDNA damageDNA repairBiologymedicine.disease_causeCockayne syndromemedicineAnimalsHumansCockayne SyndromePoly-ADP-Ribose Binding ProteinsMutationDNA HelicasesBase excision repairmedicine.diseaseMolecular biologyCell biologyDNA Repair EnzymesMitochondrial DNA repairMutationDNA mismatch repairOxidation-ReductionDNA DamageTranscription FactorsDevelopmental BiologyNucleotide excision repairMechanisms of Ageing and Development
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Up-Regulation of leucocytes Genes Implicated in Telomere Dysfunction and Cellular Senescence Correlates with Depression and Anxiety Severity Scores

2012

BACKGROUND: Major depressive disorder (MDD) is frequently associated with chronic medical illness responsible of increased disability and mortality. Inflammation and oxidative stress are considered to be the major mediators of the allostatic load, and has been shown to correlate with telomere erosion in the leucocytes of MDD patients, leading to the model of accelerated aging. However, the significance of telomere length as an exclusive biomarker of aging has been questioned on both methodological and biological grounds. Furthermore, telomeres significantly shorten only in patients with long lasting MDD. Sensitive and dynamic functional biomarkers of aging would be clinically useful to eval…

AgingGene Expressionlcsh:MedicineAnxietySocial and Behavioral Sciences0302 clinical medicineBiomarkers of agingMolecular Cell BiologyLeukocytesPathologyPsychologylcsh:ScienceCellular SenescenceDepression (differential diagnoses)Psychiatry0303 health sciencesMultidisciplinaryDepressionChromosome BiologyGenomicsMiddle AgedTelomereAllostatic loadUp-RegulationTelomeresMental HealthMedicineMajor depressive disorderAnxietyBiomarker (medicine)Femalemedicine.symptomResearch ArticleAdultSenescenceClinical PathologyPsychological StressBiologybehavioral disciplines and activitiesMolecular Genetics03 medical and health sciencesDiagnostic Medicinemental disordersGeneticsmedicineHumansBiologyCyclin-Dependent Kinase Inhibitor p16030304 developmental biologyDepressive Disorder Majorlcsh:RComputational BiologyHuman GeneticsDNAmedicine.diseaseTelomereOxygenGene Expression RegulationImmunologyStathminlcsh:QBiomarkers030217 neurology & neurosurgeryDNA DamagePLoS ONE
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Mitochondria, oxidative stress and aging

2000

In the eighties, Miquel and Fleming suggested that mitochondria play a key role in cellular aging. Mitochondria, and specially mitochondrial DNA (mtDNA), are major targets of free radical attack. At present, it is well established that mitochondrial deficits accumulate upon aging due to oxidative damage. Thus, oxidative lesions to mtDNA accumulate with age in human and rodent tissues. Furthermore, levels of oxidative damage to mtDNA are several times higher than those of nuclear DNA. Mitochondrial size increases whereas mitochondrial membrane potential decreases with age in brain and liver. Recently, we have shown that treatment with certain antioxidants, such as sulphur-containing antioxid…

AgingMitochondrial DNAFree RadicalsDNA damageAge FactorsGeneral MedicineOxidative phosphorylationBiologyMitochondrionMitochondrial Sizemedicine.disease_causeBiochemistryAntioxidantsMitochondriaLipid peroxidationOxidative Stresschemistry.chemical_compoundBiochemistrychemistrymedicineReactive Oxygen SpeciesOxidative stressDNA DamageFree-radical theory of agingFree Radical Research
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Age-Related Changes of Liver Antioxidant Enzymes and 8-Hydroxy-2-Deoxyguanosine During Fetal–Neonate Transition and Early Rat Development

2000

We have studied the pro-antioxidant status of the rat liver on the last day of gestation and at 1, 15, and 30 days of extrauterine life. Representative variables, such as activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase and concentrations of reduced glutathione and 8-hydroxy-2'-deoxyguanosine, were determined in liver to assess the degree of birth-associated oxidative stress during the fetal-neonatal transition and early development of the rat. Percentages by which liver Cu/ZnSOD activity increased over the basal value of the fetal liver were 54%, 95%, and 127% at neonatal days 1, 15, and 30, respectively. There was a lack of induction in the development profil…

Agingmedicine.medical_specialtyAntioxidantmedicine.medical_treatmentClinical Biochemistrymedicine.disease_causeBiochemistryAntioxidantsSuperoxide dismutasechemistry.chemical_compoundFetusPregnancyInternal medicineGeneticsmedicineAnimalsDeoxyguanosineRats WistarMolecular Biologychemistry.chemical_classificationGlutathione PeroxidaseFetusbiologySuperoxide DismutaseGlutathione peroxidaseDeoxyguanosineCell BiologyGlutathioneCatalaseGlutathioneRatsOxidative StressEndocrinologyAnimals NewbornLiverchemistry8-Hydroxy-2'-DeoxyguanosineCatalasebiology.proteinFemaleOxidative stressDNA DamageIUBMB Life (International Union of Biochemistry and Molecular Biology: Life)
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The Effect of Moderate- Versus High-Intensity Resistance Training on Systemic Redox State and DNA Damage in Healthy Older Women

2018

This study investigated effects of a 16-week progressive resistance training program (RTP) with elastic bands at two different intensities on systemic redox state, DNA damage, and physical function in healthy older women. Methods: Participants were randomly assigned to the high-intensity group (HIGH; n = 39), moderate-intensity group (MOD; n = 31), or control group (CG; n = 23). The exercise groups performed an RTP twice a week with three to four sets of 6 (HIGH) or 15 (MOD) repetitions of six overall body exercises at a perceived exertion rate of 8–9 on the OMNI-Resistance Exercise Scale for use with elastic bands. Thiol redox state was determined by reduced glutathione (GSH), oxidized gl…

Agingmedicine.medical_specialtyDNA damageStrength trainingEstrès oxidatiuUrinemedicine.disease_causeRedox03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicinemedicineHumansDeoxyguanosineAgedAged 80 and overResearch and TheoryResistance trainingResistance Training030229 sport sciencesGlutathioneMiddle AgedEntrenament (Esport)GlutathioneHealthy VolunteersExercise TherapyEndocrinologychemistryFemaleOxidation-Reduction030217 neurology & neurosurgeryOxidative stressDNA Damage
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Exposure to gp120 of HIV-1 induces an increased release of arachidonic acid in rat primary neuronal cell culture followed by NMDA receptor-mediated n…

1995

After incubation of highly enriched neurons from rat cerebral cortex with the HIV-1 coat protein gp120 for 18 h, cells showed fragmentation of DNA at internucleosomal linkers followed by NMDA receptor-mediated neurotoxicity. We report that in response to exposure to gp120 cells react with an increased release of arachidonic acid (AA) via activation of phospholipase A2. This process was not inhibited by NMDA receptor antagonists. To investigate the role of AA on the sensitivity of the NMDA receptor towards its agonist, low concentrations of NMDA were co-administered with AA. This condition enhanced the NMDA-mediated cytotoxicity. Administration of mepacrine reduced cytotoxicity caused by gp1…

Agonistmedicine.drug_classNeurotoxinsPharmacologyHIV Envelope Protein gp120Receptors N-Methyl-D-Aspartatechemistry.chemical_compoundPhospholipase A2medicineAnimalsFragmentation (cell biology)Rats WistarCytotoxicityCells CulturedNeuronsArachidonic AcidbiologyCell DeathGeneral NeuroscienceNeurotoxicitymedicine.diseaseRatsnervous systemchemistryCell cultureQuinacrinebiology.proteinHIV-1NMDA receptorArachidonic acidDNA DamageThe European journal of neuroscience
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Assessment of mechanisms driving non-linear dose-response relationships in genotoxicity testing.

2014

In genetic toxicology, risk assessment has traditionally adopted linear dose-responses for any compound that causes genotoxic effects. Increasing evidence of non-linear dose-responses, however, suggests potential cellular tolerance to low levels of many genotoxicants with diverse modes of action. Such putative non-linear dose-responses need to be substantiated by strong mechanistic data that identifies the mechanisms responsible for the tolerance to low doses. This can be achieved by experimental demonstration of cytoprotective mechanisms and by providing experimental support for the existence of tolerance mechanisms against low dose effects. By highlighting key experiments into low dose me…

Alkylating AgentsDNA repairmedicine.drug_classTopoisomerase InhibitorsHealth Toxicology and MutagenesisTransgeneComputational biologyBiologyRisk AssessmentGenotoxicity testingToxicologyGeneticsmedicineAnimalsHumansGene knockoutDose-Response Relationship DrugMutagenicity TestsLow doseNucleosidesAneugensOxidantsModels ChemicalParticulate MatterTopoisomerase inhibitorGenetic ToxicologyDNA DamageMutagensMutation research. Reviews in mutation research
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