Search results for " nitrogen"

showing 10 items of 319 documents

Peripheral artery disease, redox signaling, oxidative stress – Basic and clinical aspects

2017

Reactive oxygen and nitrogen species (ROS and RNS, e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. At higher concentrations, ROS and RNS lead to oxidative stress and oxidative damage of biomolecules (e.g. via formation of peroxynitrite, fenton chemistry). Peripheral artery disease (PAD) is characterized by severe ischemic conditions in the periphery leading to intermittent claudication and critical limb ischemia (end stage). It is well known that redox biology and oxidative stress play an important role in this setting. We here discuss the major pathways of oxidative stress and re…

0301 basic medicineAntioxidantRedox signalingmedicine.medical_treatmentCellular differentiationClinical BiochemistryReview Article030204 cardiovascular system & hematologyPharmacologymedicine.disease_causeBiochemistrychemistry.chemical_compound0302 clinical medicineGene Regulatory Networks610 Medicine & healthlcsh:QH301-705.5chemistry.chemical_classificationlcsh:R5-920Anticholesteremic AgentsReactive Nitrogen Speciesmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionPeroxynitriteSignal Transductionmedicine.medical_specialtyCell signalingAntioxidant therapy610 Medicine & healthNitric oxide03 medical and health sciencesPeripheral Arterial DiseasemedicineHumansExerciseReactive oxygen speciesbusiness.industryOrganic ChemistryClaudication and critical limb ischemiaWalking distanceIntermittent claudicationSurgeryOxidative Stress030104 developmental biologychemistrylcsh:Biology (General)Peripheral artery (occlusive) diseasebusinessReactive Oxygen SpeciesOxidative stressRedox Biology
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Regulation of vascular function and inflammation via cross talk of reactive oxygen and nitrogen species from mitochondria or nadph oxidase—implicatio…

2020

Oxidative stress plays a key role for the development of cardiovascular, metabolic, and neurodegenerative disease. This concept has been proven by using the approach of genetic deletion of reactive oxygen and nitrogen species (RONS) producing, pro-oxidant enzymes as well as by the overexpression of RONS detoxifying, antioxidant enzymes leading to an amelioration of the severity of diseases. Vice versa, the development and progression of cardiovascular diseases is aggravated by overexpression of RONS producing enzymes as well as deletion of RONS detoxifying enzymes. We have previously identified cross talk mechanisms between different sources of RONS, which can amplify the oxidative stress-m…

0301 basic medicineAntioxidantmedicine.medical_treatmentReview030204 cardiovascular system & hematologyMitochondrionmedicine.disease_causelcsh:Chemistry0302 clinical medicineEndothelial dysfunctionEndothelial dysfunctionlcsh:QH301-705.5SpectroscopyNADPH oxidasebiologyChemistryGeneral MedicineReactive Nitrogen SpeciesComputer Science ApplicationsCell biologyMitochondriaCardiovascular DiseasesDisease Progressionmedicine.symptomInflammationENOS uncouplingOxidative phosphorylationEndothelial dysfunction; ENOS uncoupling; Kindling radicals; Low-grade inflammation; Mitochondria; NADPH oxidase; Oxidative stress; Redox cross talkLow-grade inflammationCatalysisRedox cross talkInorganic Chemistry03 medical and health sciencesmedicineDiabetes MellitusAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyInflammationNADPH oxidaseOrganic ChemistryNADPH Oxidasesmedicine.diseaseAngiotensin II030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Oxidative stressbiology.proteinKindling radicalsReactive Oxygen SpeciesOxidative stress
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Oxidative Stress, a Crossroad Between Rare Diseases and Neurodegeneration

2020

Oxidative stress is an imbalance between production and accumulation of oxygen reactive species and/or reactive nitrogen species in cells and tissues, and the capacity of detoxifying these products, using enzymatic and non-enzymatic components, such as glutathione. Oxidative stress plays roles in several pathological processes in the nervous system, such as neurotoxicity, neuroinflammation, ischemic stroke, and neurodegeneration. The concepts of oxidative stress and rare diseases were formulated in the eighties, and since then, the link between them has not stopped growing. The present review aims to expand knowledge in the pathological processes associated with oxidative stress underlying …

0301 basic medicineAtaxiaUnverricht–Lundborg disease (ULD)PhysiologyNeurodegeneration with brain iron accumulationClinical BiochemistryFriedreich’s ataxiaReviewmedicine.disease_causeBioinformaticsBiochemistry03 medical and health scienceschemistry.chemical_compoundLafora disease (LD)0302 clinical medicineMedicineprogressive myoclonus epilepsy (PME)Molecular BiologyNeuroinflammationReactive nitrogen speciesneurodegenerative disorders with brain iron accumulation (NBIA)business.industryNeurodegenerationlcsh:RM1-950NeurotoxicityCell Biologymedicine.diseaseDravet syndromeCharcot-Marie-Tooth disease (CMT)030104 developmental biologylcsh:Therapeutics. Pharmacologychemistrymedicine.symptombusinessMyoclonusinherited retinal dystrophy (IRD)030217 neurology & neurosurgeryOxidative stressAntioxidants
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Oxidative stress and antioxidants in the pathophysiology of malignant melanoma.

2018

Abstract The high number of somatic mutations in the melanoma genome associated with cumulative ultra violet (UV) exposure has rendered it one of the most difficult of cancers to treat. With new treatment approaches based on targeted and immune therapies, drug resistance has appeared as a consistent problem. Redox biology, including reactive oxygen and nitrogen species (ROS and RNS), plays a central role in all aspects of melanoma pathophysiology, from initiation to progression and to metastatic cells. The involvement of melanin production and UV radiation in ROS/RNS generation has rendered the melanocytic lineage a unique system for studying redox biology. Overall, an elevated oxidative st…

0301 basic medicineBiochemistry & Molecular BiologyClinical Biochemistrymedicine.disease_causeBiochemistryAntioxidantsMelanin03 medical and health scienceschemistry.chemical_compound0302 clinical medicineMedicineAnimalsHumanstumor microenvironmentEpigeneticsmetastasesMolecular BiologyMelanomaReactive nitrogen specieschemistry.chemical_classificationreactive oxygen speciesReactive oxygen speciesTumor microenvironmentskin cancerbusiness.industryMelanomaintracellular redox statemedicine.diseaseOxidative Stress030104 developmental biologyreactive nitrogen specieschemistry030220 oncology & carcinogenesisCancer researchBiochemistry and Cell BiologySkin cancerbusinessOxidation-ReductionOxidative stressSignal Transduction
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New 1,4-Dihydropyridines Down-regulate Nitric Oxide in Animals with Streptozotocin-induced Diabetes Mellitus and Protect Deoxyribonucleic Acid agains…

2015

Diabetes mellitus (DM) and its complications cause numerous health and social problems throughout the world. Pathogenic actions of nitric oxide (NO) are responsible to a large extent for development of complications of DM. Search for compounds regulating NO production in patients with DM is thus important for the development of pharmacological drugs. Dihydropyridines (1,4-DHPs) are prospective compounds from this point of view. The goals of this study were to study the in vivo effects of new DHPs on NO and reactive nitrogen and oxygen species production in a streptozotocin (STZ)-induced model of DM in rats and to study their ability to protect DNA against nocive action of peroxynitrite. STZ…

0301 basic medicineBlood GlucoseMaleDihydropyridinesNitric Oxide Synthase Type IIIXanthine DehydrogenaseDown-RegulationNitric Oxide Synthase Type IIDHPS030204 cardiovascular system & hematologyPharmacologyToxicologyEndothelial NOSKidneyNitric OxideProtective AgentsNitric oxideDiabetes Mellitus Experimental03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePeroxynitrous AcidmedicineAnimalsRats WistarReactive nitrogen speciesPharmacologybiologyGeneral MedicineDNAStreptozotocinReactive Nitrogen SpeciesRatsNitric oxide synthasePeroxynitrous acid030104 developmental biologyBiochemistrychemistryLiverbiology.proteinReactive Oxygen SpeciesPeroxynitritemedicine.drugBasicclinical pharmacologytoxicology
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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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1,3,5-Triazines: A promising scaffold for anticancer drugs development

2017

This review covering literature reports from the beginning of this century to 2016 describes the synthetic pathways, the antitumor activity, the structure-activity relationship and, whenever reported, the possible mechanism of action of 1,3,5-triazine derivatives as well as of their hetero-fused compounds. Many 1,3,5-triazine derivatives, both uncondensed and hetero-fused, have shown remarkable antitumor activities and some of them reached clinical development.

0301 basic medicineModels MolecularScaffold31Disubstituted 135-triazineTrisubstituted 135-triazineAntineoplastic AgentsChemistry Techniques Synthetic01 natural sciences03 medical and health sciencesStructure-Activity RelationshipNeoplasmsDrug DiscoverymedicineAnimalsHumans5-TriazinesTrisubstituted 1Disubstituted 1Antitumor activityPharmacologyHeterofused 135-triazine010405 organic chemistryChemistryTriazinesNitrogen heterocyclesDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryGeneral MedicineHeterofused 1Combinatorial chemistry135-Triazine0104 chemical sciences030104 developmental biologyNitrogen heterocycleMechanism of action1; 3; 5-Triazines; Antitumor activity; Disubstituted 1; 3; 5-triazines; Heterofused 1; 3; 5-triazines; Nitrogen heterocycles; Trisubstituted 1; 3; 5-triazines; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Organic Chemistrymedicine.symptomAntitumor activity
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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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