0000000000362186

AUTHOR

Johanna Müller

showing 5 related works from this author

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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AT1-receptor blockade by telmisartan upregulates GTP-cyclohydrolase I and protects eNOS in diabetic rats.

2008

Several enzymatic sources of reactive oxygen species (ROS) were described as potential reasons of eNOS uncoupling in diabetes mellitus. In the present study, we investigated the effects of AT1-receptor blockade with chronic telmisartan (25 mg/kg/day, 6.5 weeks) therapy on expression of the BH4-synthesizing enzyme GTP-cyclohydrolase I (GCH-I), eNOS uncoupling, and endothelial dysfunction in streptozotocin (STZ, 60 mg/kg iv, 7 weeks)-induced diabetes mellitus (type I). Telmisartan therapy did not modify blood glucose and body weight. Aortas from diabetic animals had vascular dysfunction as revealed by isometric tension studies (acetylcholine and nitroglycerin potency). Vascular and cardiac RO…

Blood GlucoseMalemedicine.medical_specialtyNitric Oxide Synthase Type IIImedicine.disease_causeBiochemistryBenzoatesReceptor Angiotensin Type 1chemistry.chemical_compoundEnosPhysiology (medical)Internal medicinemedicineDiabetes MellitusAnimalsTelmisartanEndothelial dysfunctionRats WistarXanthine oxidaseGTP CyclohydrolaseNADPH oxidasebiologySuperoxideBody WeightNADPH Oxidasesmedicine.diseaseStreptozotocinbiology.organism_classificationMitochondriaRatsUp-RegulationEnzyme ActivationOxidative StressEndocrinologychemistrybiology.proteinBenzimidazolesTelmisartanAngiotensin II Type 1 Receptor BlockersOxidative stressmedicine.drugFree radical biologymedicine
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Chemical model systems for cellular nitros(yl)ation reactions.

2009

S-nitros(yl)ation belongs to the redox-based posttranslational modifications of proteins but the underlying chemistry is controversial. In contrast to current concepts involving the autoxidation of nitric oxide ( • NO, nitrogen monoxide), we and others have proposed the formation of peroxynitrite (oxoperoxonitrate (1-)) as an essential intermediate. This requires low cellular fluxes of 'NO and superoxide ( • O 2 - ), for which model systems have been introduced. We here propose two new systems for nitros(yl)ation that avoid the shortcomings of previous models. Based on the thermal decomposition of 3-morpholinosydnonimine, equal fluxes of • NO and • O 2 - were generated and modulated by the …

StereochemistrySwineNitrosationIn Vitro TechniquesPhotochemistryNitric OxideBiochemistryRedoxArticlechemistry.chemical_compoundElectrophilic substitutionPhysiology (medical)Peroxynitrous AcidAnimalsAutoxidationPhenolNitrosoniumSuperoxideSuperoxide DismutaseGlutathioneIsocitrate DehydrogenasePeroxynitrous acidchemistryModels ChemicalMolsidomineNitrosationCattlePeroxynitriteFree radical biologymedicine
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ALDH-2 deficiency increases cardiovascular oxidative stress--evidence for indirect antioxidative properties.

2007

Abstract Mitochondrial aldehyde dehydrogenase (ALDH-2) reduces reactive oxygen species (ROS) formation related to toxic aldehydes; additionally, it provides a bioactivating pathway for nitroglycerin. Since acetaldehyde, nitroglycerin, and doxorubicin treatment provoke mitochondrial oxidative stress, we used ALDH-2−/− mice and purified recombinant human ALDH-2 to test the hypothesis that ALDH-2 has an indirect antioxidant function in mitochondria. Antioxidant capacity of purified ALDH-2 was comparable to equimolar doses of glutathione, cysteine, and dithiothreitol; mitochondrial oxidative stress was comparable in C57Bl6 and ALDH-2−/− mice after acute challenges with nitroglycerin or doxorubi…

Mitochondrial ROSAntioxidantmedicine.medical_treatmentBiophysicsAldehyde dehydrogenaseAcetaldehydeMitochondrionPharmacologymedicine.disease_causeBiochemistryCardiovascular SystemModels BiologicalAntioxidantschemistry.chemical_compoundMiceNitroglycerinmedicineAnimalsHumansCysteineMolecular Biologychemistry.chemical_classificationReactive oxygen speciesbiologyDose-Response Relationship DrugAldehyde Dehydrogenase MitochondrialAcetaldehydeCell BiologyGlutathioneAldehyde DehydrogenaseGlutathioneMitochondriaMice Inbred C57BLDithiothreitolOxidative StresschemistryBiochemistryDoxorubicincardiovascular systembiology.proteinReactive Oxygen SpeciesOxidative stressBiochemical and biophysical research communications
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First Evidence for a Crosstalk Between Mitochondrial and NADPH Oxidase-Derived Reactive Oxygen Species in Nitroglycerin-Triggered Vascular Dysfunction

2008

Chronic nitroglycerin treatment results in development of nitrate tolerance associated with endothelial dysfunction (ED). We sought to clarify how mitochondria- and NADPH oxidase (Nox)-derived reactive oxygen species (ROS) contribute to nitrate tolerance and nitroglycerin-induced ED. Nitrate tolerance was induced by nitroglycerin infusion in male Wistar rats (100 microg/h/4 day) and in C57/Bl6, p47(phox/) and gp91(phox/) mice (50 microg/h/4 day). Protein and mRNA expression of Nox subunits were unaltered by chronic nitroglycerin treatment. Oxidative stress was determined in vascular rings and mitochondrial fractions of nitroglycerin-treated animals by L-012 enhanced chemiluminescence, revea…

MalePhysiologyVasodilator AgentsClinical BiochemistryMitochondrionPharmacologymedicine.disease_causeBiochemistryMitochondria HeartMiceNitroglycerinchemistry.chemical_compoundEthidiumAortaChromatography High Pressure LiquidHeart metabolismGeneral Environmental Sciencechemistry.chemical_classificationNADPH oxidasebiologyReverse Transcriptase Polymerase Chain ReactionReactive Nitrogen SpeciesBiochemistryCyclosporinecardiovascular systemcirculatory and respiratory physiologyBlotting WesternIn Vitro TechniquesTransfectionCell LineRotenonemedicineAnimalsHumansRNA MessengerRats WistarMolecular BiologyReactive oxygen speciesNADPH OxidasesCell BiologyRotenoneRatsMice Inbred C57BLchemistryMitochondrial permeability transition poreVasoconstrictionApocyninbiology.proteinGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidative stressAntioxidants & Redox Signaling
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