Search results for "Reactive nitrogen"

showing 10 items of 74 documents

Modification of DNA structure by reactive nitrogen species as a result of 2-methoxyestradiol–induced neuronal nitric oxide synthase uncoupling in met…

2020

Abstract 2-methoxyestradiol (2-ME) is a physiological anticancer compound, metabolite of 17β-estradiol. Previously, our group evidenced that from mechanistic point of view one of anticancer mechanisms of action of 2-ME is specific induction and nuclear hijacking of neuronal nitric oxide synthase (nNOS), resulting in local generation of nitro-oxidative stress and finally, cancer cell death. The current study aims to establish the substantial mechanism of generation of reactive nitrogen species by 2-ME. We further achieved to identify the specific reactive nitrogen species involved in DNA-damaging mechanism of 2-ME. The study was performed using metastatic osteosarcoma 143B cells. We detected…

0301 basic medicineDNA damageClinical BiochemistryBone NeoplasmsNitric Oxide Synthase Type INitric OxideBiochemistryNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePeroxynitrous AcidHumansMTT assayViability assaylcsh:QH301-705.5Reactive nitrogen speciesSettore CHIM/02 - Chimica FisicaOsteosarcomalcsh:R5-920Settore BIO/16 - Anatomia UmanaOrganic ChemistryDNAReactive Nitrogen Species2-MethoxyestradiolPeroxynitrous acid030104 developmental biologychemistrylcsh:Biology (General)Settore CHIM/03 - Chimica Generale E InorganicaCancer cellBiophysicslcsh:Medicine (General)030217 neurology & neurosurgeryPeroxynitrite2 methoxyestradiol nitric oxide chemotherapyResearch PaperRedox Biology
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The purine analogues abacavir and didanosine increase acetaminophen-induced hepatotoxicity by enhancing mitochondrial dysfunction

2016

Background NRTIs are essential components of HIV therapy with well-documented, long-term mitochondrial toxicity in hepatic cells, but whose acute effects on mitochondria are unclear. As acetaminophen-induced hepatotoxicity also involves mitochondrial interference, we hypothesized that it would be exacerbated in the context of ART. Methods We evaluated the acute effects of clinically relevant concentrations of the most widely used NRTIs, alone or combined with acetaminophen, on mitochondrial function and cellular viability. Results The purine analogues abacavir and didanosine produced an immediate and concentration-dependent inhibition of oxygen consumption and complex I and III activity. Th…

0301 basic medicineMicrobiology (medical)Mitochondrial DiseasesstavudineAnti-HIV Agentsantiretroviral therapyPurine analogueContext (language use)Mitochondria LiverMitochondrionPharmacologymedicine.disease_causeacute liver-failureCell Line03 medical and health sciencesOxygen ConsumptionmedicineHumansPharmacology (medical)Reverse-transcriptase inhibitorsAcetaminophenPharmacologychemistry.chemical_classificationmechanismsReactive oxygen speciesbusiness.industryassociationtoxicityAnalgesics Non-Narcoticmedicine.diseaseGlutathioneReactive Nitrogen SpeciesDideoxynucleosideshep3b cellsAcetaminophenMitochondrial toxicityDidanosine030104 developmental biologyInfectious DiseaseschemistryElectron Transport Chain Complex ProteinsToxicityhypersensitivityChemical and Drug Induced Liver Injurybusinesshepatic cellsOxidative stressmedicine.drug
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Redox regulation of cardiovascular inflammation – Immunomodulatory function of mitochondrial and Nox-derived reactive oxygen and nitrogen species

2017

Oxidative stress is a major hallmark of cardiovascular diseases although a causal link was so far not proven by large clinical trials. However, there is a close association between oxidative stress and inflammation and increasing evidence for a causal role of (low-grade) inflammation for the onset and progression of cardiovascular diseases, which may serve as the missing link between oxidative stress and cardiovascular morbidity and mortality. With the present review we would like to highlight the multiple redox regulated pathways in inflammation, discuss the sources of reactive oxygen and nitrogen species that are of interest for these processes and finally discuss the importance of angiot…

0301 basic medicineNeutrophilsInflammationmedicine.disease_causeCardiovascular SystemExtracellular TrapsBiochemistrystat03 medical and health scienceschemistry.chemical_compoundPhysiology (medical)medicineHumansEndothelial dysfunctionInflammationMitoQChemistryAngiotensin IIEndothelial CellsNADPH OxidasesNF-κBmedicine.diseaseReactive Nitrogen SpeciesAngiotensin IIMitochondriaOxidative Stress030104 developmental biologyGene Expression RegulationCardiovascular DiseasesTRIFImmunologymedicine.symptomReactive Oxygen SpeciesOxidation-ReductionOxidative stressSignal TransductionFree Radical Biology and Medicine
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Carnosine protects pancreatic beta cells and islets against oxidative stress damage

2018

Abstract Islet transplantation is a valid therapeutic option for type 1 diabetes treatment. However, in this procedure one of the major problems is the oxidative stress produced during pancreatic islet isolation. The aim of our study was to evaluate potential protective effects of L-carnosine and its isomer D-carnosine against oxidative stress. We evaluated the carnosine effect on cell growth, cell death, insulin production, and the main markers of oxidative stress in rat and murine stressed beta cell lines as well as in human pancreatic islets. Both isomers clearly inhibited hydrogen peroxide induced cytotoxicity, with a decrease in intracellular reactive oxygen and nitrogen species, preve…

0301 basic medicineNitrous OxideCarnosineApoptosismedicine.disease_causeBiochemistrychemistry.chemical_compoundMice0302 clinical medicineEndocrinologyInsulin-Secreting CellsInsulin Secretiongeography.geographical_feature_categoryChemistryNitrotyrosineCarnosineDiabetesIsletReactive Nitrogen Speciesmedicine.anatomical_structureBeta cellPancreatic islet transplantationmedicine.medical_specialtyCell SurvivalProtective AgentsCell Line03 medical and health sciencesInternal medicinemedicineAnimalsHumansMolecular BiologyBeta cell lineCell ShapeCell ProliferationSettore MED/04 - Patologia GeneralegeographyPancreatic isletsTranscription Factor RelAHydrogen PeroxideRatsTransplantationOxidative Stress030104 developmental biologyEndocrinologyGlucoseGene Expression RegulationCytoprotectionTyrosinePancreatic islet transplantationReactive Oxygen Species030217 neurology & neurosurgeryOxidative stressBiomarkers
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Crosstalk of mitochondria with NADPH oxidase via reactive oxygen and nitrogen species signalling and its role for vascular function

2016

Cardiovascular diseases are associated with and/or caused by oxidative stress. This concept has been proven by using the approach of genetic deletion of reactive species producing (pro-oxidant) enzymes as well as by the overexpression of reactive species detoxifying (antioxidant) enzymes leading to a marked reduction of reactive oxygen and nitrogen species (RONS) and in parallel to an amelioration of the severity of diseases. Likewise, the development and progression of cardiovascular diseases is aggravated by overexpression of RONS producing enzymes as well as deletion of antioxidant RONS detoxifying enzymes. Thus, the consequences of the interaction (redox crosstalk) of superoxide/hydroge…

0301 basic medicinePharmacologychemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseAntioxidantbiologySuperoxidemedicine.medical_treatmentMitochondrionmedicine.disease_cause03 medical and health scienceschemistry.chemical_compoundCrosstalk (biology)030104 developmental biologychemistryBiochemistrybiology.proteinmedicineReactive nitrogen speciesOxidative stressBritish Journal of Pharmacology
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Taking up the cudgels for the traditional reactive oxygen and nitrogen species detection assays and their use in the cardiovascular system

2017

Reactive oxygen and nitrogen species (RONS such as H2O2, nitric oxide) confer redox regulation of essential cellular functions (e.g. differentiation, proliferation, migration, apoptosis), initiate and catalyze adaptive stress responses. In contrast, excessive formation of RONS caused by impaired break-down by cellular antioxidant systems and/or insufficient repair of the resulting oxidative damage of biomolecules may lead to appreciable impairment of cellular function and in the worst case to cell death, organ dysfunction and severe disease phenotypes of the entire organism. Therefore, the knowledge of the severity of oxidative stress and tissue specific localization is of great biological …

0301 basic medicineProgrammed cell deathRedox signalingClinical BiochemistrySevere diseaseReview ArticleBiologymedicine.disease_causeCardiovascular SystemBiochemistry03 medical and health sciencesPhysiology (medical)medicineDihydroethidium oxidative fluorescence microtopographyAnimalsHumanslcsh:QH301-705.5Organismchemistry.chemical_classificationlcsh:R5-920Reactive oxygen speciesFluorescence and chemiluminescence-based assaysOrganic ChemistrySpecies detectionNADPH OxidasesPhenotypeReactive Nitrogen SpeciesOxidative Stress030104 developmental biologylcsh:Biology (General)chemistryBiochemistryL-012-enhanced chemiluminescenceLuminescent MeasurementsLucigenin-enhanced chemiluminescencelcsh:Medicine (General)Reactive Oxygen SpeciesNeuroscienceOxidation-ReductionFunction (biology)Oxidative stressFree Radical Biology and Medicine
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Oxidative post‐translational modifications in histones

2019

Epigenetic regulation is attracting much attention because it explains many of the effects that the external environment induces in organisms. Changes in the cellular redox status and even more specifically in its nuclear redox compartment is one of these examples. Redox changes can induce modulation of the epigenetic regulation in cells. Here we present a few cases where reactive oxygen or nitrogen species induces epigenetic marks in histones. Posttranslational modification of these proteins like histone nitrosylation, carbonylation, or glutathionylation together with other mechanisms not reviewed here are the cornerstones of redox-related epigenetic regulation. We currently face a new fie…

0301 basic medicineProtein CarbonylationClinical BiochemistryOxidative phosphorylationmedicine.disease_causeBiochemistryEpigenesis GeneticHistonesProtein CarbonylationMice03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansEpigeneticsEpigenesisSulfur CompoundsbiologyChemistryNitrosylationGeneral MedicineGlutathioneReactive Nitrogen SpeciesCell biologyOxidative Stress030104 developmental biologyHistone030220 oncology & carcinogenesisbiology.proteinMolecular MedicineSignal transductionReactive Oxygen SpeciesOxidation-ReductionProtein Processing Post-TranslationalOxidative stressNitroso CompoundsSignal TransductionBioFactors
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Corrigendum to “European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS…

2018

The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics b…

0301 basic medicineSocieties ScientificRedox signalingInternational CooperationClinical BiochemistryNanotechnologyReview ArticleBiologyPublic administrationBiochemistryAntioxidantsArticle03 medical and health sciencesmedia_common.cataloged_instanceAnimalsHumansCost actionEuropean UnionEuropean unionMolecular Biologylcsh:QH301-705.5media_commonFunding AgencyRedox therapeuticslcsh:R5-920Organic ChemistryReactive nitrogen species030104 developmental biologyWork (electrical)lcsh:Biology (General)Oxidative stressReactive Oxygen Specieslcsh:Medicine (General)Oxidation-ReductionSignal TransductionRedox Biology
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Cytomics of Oxidative Stress: Probes and Problems

2017

Oxidative stress has been implicated in cellular senescence and aging, as well as in the onset and progression of many diverse genetic and acquired diseases and conditions. However, reactive oxygen (ROS) and nitrogen (RNS) species initiating oxidative stress also serve important regulatory roles, mediated by intercellular and intracellular signaling, adaptation to endogenous and exogenous stress, and destruction of invading pathogens. Fluorescence-based analysis of oxidative stress and related processes is an important cytomic application; almost 4000 papers were published between 1989 and 2016. To ascertain the specific role of ROS and RNS in oxidative stress studies by cytomic methodologi…

0301 basic medicinechemistry.chemical_classificationReactive oxygen speciesAcquired diseasesCellular senescenceEndogenyBiologymedicine.disease_causeCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinechemistry030220 oncology & carcinogenesismedicineCytomicsIntracellularReactive nitrogen speciesOxidative stress
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Real-time cytometric assay of nitric oxide and superoxide interaction in peripheral blood monocytes: A no-wash, no-lyse kinetic method

2015

Background Nitric oxide (NO) and its related reactive nitrogen species (RNS) and reactive oxygen species (ROS) are crucial in monocyte responses against pathogens and also in inflammatory conditions. Central to both processes is the generation of the strong oxidant peroxynitrite (ONOO) by a fast reaction between NO and superoxide anion. ONOO is a biochemical junction for ROS- and RNS cytotoxicity and causes protein nitrosylation. Circulating by-products of protein nitrosylation are early biomarkers of inflammation-based conditions, including minimal hepatic encephalopathy in cirrhotic patients (Montoliu et al., Am J Gastroenterol 2011; 106:1629–1637). In this context, we have designed a nov…

0301 basic medicinechemistry.chemical_classificationReactive oxygen speciesHistologymedicine.diagnostic_testProtein nitrosylationSuperoxideContext (language use)Cell BiologyMolecular biologyPathology and Forensic MedicineNitric oxideFlow cytometry03 medical and health scienceschemistry.chemical_compound030104 developmental biologychemistryBiochemistrymedicinePeroxynitriteReactive nitrogen speciesCytometry Part B: Clinical Cytometry
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