Search results for "oxides"

showing 10 items of 547 documents

Ursodeoxycholic acid protects against secondary biliary cirrhosis in rats by preventing mitochondrial oxidative stress

2004

Ursodeoxycholic acid (UDCA) improves clinical and biochemical indices in primary biliary cirrhosis and prolongs survival free of liver transplantation. Recently, it was suggested that the cytoprotective mechanisms of UDCA may be mediated by protection against oxidative stress, which is involved in the development of cirrhosis induced by chronic cholestasis. The aims of the current study were 1) to identify the mechanisms involved in glutathione depletion, oxidative stress, and mitochondrial impairment during biliary cirrhosis induced by chronic cholestasis in rats; and 2) to determine the mechanisms associated with the protective effects of UDCA against secondary biliary cirrhosis. The find…

Malemedicine.medical_specialtyCirrhosisCardiolipinsGlutamate-Cysteine LigaseBiliary cirrhosisPopulationBiologymedicine.disease_causeMembrane Potentialschemistry.chemical_compoundPrimary biliary cirrhosisInternal medicinemedicineCardiolipinAnimalsRats Wistareducationeducation.field_of_studyCholestasisHepatologyLiver Cirrhosis BiliaryUrsodeoxycholic AcidCystathionine gamma-LyaseGlutathionemedicine.diseaseGlutathioneUrsodeoxycholic acidMitochondriaPeroxidesRatsOxidative StressEndocrinologyLiverchemistryChronic DiseaseHepatocytesOxidation-ReductionOxidative stressmedicine.drugHepatology
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REDUCED OXIDATIVE STRESS DURING ACELLULAR REPERFUSION OF THE RAT LIVER AFTER HYPOTHERMIC OSCILLATING PERFUSION

1999

Background ATP resynthesis during reperfusion after liver preservation has been shown to be well correlated with the function of transplanted grafts. Nevertheless, the advantages of a cellular energy charge loading during the preservation period are yet not fully understood. This study evaluates the effects of different nucleotide levels at the end of preservation on metabolic changes and oxidative stress during reperfusion. Methods Two experimental groups were chosen reflecting different energy charge states after preservation: static cold storage for 10 hr and hypothermic oxygenated oscillating perfusion for 10 hr. In both experimental groups, normothermic ex vivo acellular reperfusion ov…

Malemedicine.medical_specialtyCold storageHypothermiaLipid peroxidationSuperoxide dismutasechemistry.chemical_compoundSuperoxidesMalondialdehydeRats Inbred BNInternal medicinemedicineAnimalsEnergy chargeLiver preservationCryopreservationTransplantationbiologyTumor Necrosis Factor-alphaChemistrySuperoxideLiver cellOrgan PreservationMalondialdehydeLiver GlycogenRatsPerfusionOxidative StressEndocrinologyLiverBiochemistryReperfusionbiology.proteinLipid PeroxidationBiomarkersTransplantation
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Oxidant/antioxidant status in obese children compared to pediatric patients with type 1 diabetes mellitus.

2009

Codoner-Franch P, Pons-Morales S, Boix-Garcia L, Valls-Belles V. Oxidant/antioxidant status in obese children compared to pediatric patients with type 1 diabetes mellitus. Background: Type 1 diabetes (T1D) mellitus and obesity are recognized risk factors for cardiovascular disease (CVD). A common mechanism underlying an increased risk for endothelial dysfunction in these two metabolic diseases is oxidative stress. Objective: To evaluate and compare the oxidant/antioxidant defense systems in children affected with T1D or obesity in order to determine the importance of oxidative stress before the emergence of complications. Subjects: Children with T1D (n = 20) or obesity (n = 22), without com…

Malemedicine.medical_specialtyLipid PeroxidesAntioxidantErythrocytesAdolescentEndocrinology Diabetes and Metabolismmedicine.medical_treatmentalpha-TocopherolProtein oxidationmedicine.disease_causeLipid peroxidationProtein Carbonylationchemistry.chemical_compoundInternal medicineMalondialdehydeInternal MedicinemedicineHumansObesityProspective StudiesChildRetrospective Studieschemistry.chemical_classificationType 1 diabetesGlutathione Peroxidasebusiness.industryGlutathione peroxidaseMalondialdehydemedicine.diseasebeta CaroteneObesityGlutathioneOxidative StressEndocrinologyDiabetes Mellitus Type 1chemistryPediatrics Perinatology and Child HealthFemaleLipid PeroxidationbusinessOxidative stressPediatric diabetes
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Absence of lipid peroxidation as determined by ethane exhalation in rats treated with 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD).

1985

The exhalation of ethane is widely used as an indicator of in vivo lipid peroxidation. To test the hypothesis that lipid peroxidative events are involved in the toxicity of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), we administered a lethal dose of TCDD (60 μg/kg), IP to male Sprague Dawley rats (160–180 g) and measured by gas chromatography the exhalation of ethane into the atmosphere of a closed all-glass exposure chamber. TCDD-treated rats exhaled only slightly more ethane than control rats at a single time point 7 days following TCDD administration. Since the exhalation of ethane is the net result of the endogenous production of the gas and its metabolic degradation, the latter was …

Malemedicine.medical_specialtyLipid PeroxidesPolychlorinated DibenzodioxinsHealth Toxicology and MutagenesisEndogenyToxicologyDioxinsLipid peroxidationchemistry.chemical_compoundCytochrome P-450 Enzyme SystemIn vivoInternal medicinemedicineAnimalsheterocyclic compoundsEthaneChemistryLethal doseExhalationRats Inbred StrainsGeneral MedicineMetabolismTetrachlorodibenzo-p-dioxinRatsstomatognathic diseasesEndocrinologyBiochemistryToxicityArchives of toxicology
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Pregnenolone sulfate, a naturally occurring excitotoxin involved in delayed retinal cell death.

2002

The present study was designed to investigate the neurosteroid pregnenolone sulfate (PS), known for its ability to modulate NMDA receptors and interfere with acute excitotoxicity, in delayed retinal cell death. Three hours after exposure of the isolated and intact retina to a 30-min PS pulse, DNA fragmentation as assessed by genomic DNA gel electrophoresis and a modified in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method appeared concurrently with an increase in superoxide dismutase (SOD) activity and thiobarbituric acid-reactive substances (TBARS) levels. At 7 h, the increased amount of DNA laddering was accompanied by a higher number of TUN…

Malemedicine.medical_specialtyNeurotoxinsExcitotoxicityApoptosisDNA FragmentationDNA ladderingBiologymedicine.disease_causeBiochemistryReceptors N-Methyl-D-AspartateThiobarbituric Acid Reactive SubstancesRetinaCellular and Molecular Neurosciencechemistry.chemical_compoundAdjuvants ImmunologicSuperoxidesInternal medicinemedicineTBARSIn Situ Nick-End LabelingAnimalsCycloheximideRats WistarProgesteroneProtein Synthesis InhibitorsTUNEL assayEstradiolL-Lactate DehydrogenaseDehydroepiandrosterone SulfateSuperoxide DismutaseRatsEndocrinologychemistryApoptosisPregnenolonePregnenoloneDNA fragmentationLipid PeroxidationPregnenolone sulfateReactive Oxygen Speciesmedicine.drugJournal of neurochemistry
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Chronic Therapy With Isosorbide-5-Mononitrate Causes Endothelial Dysfunction, Oxidative Stress and a Marked Increase in Vascular Endothelin-1 Express…

2011

Aims Isosorbide-5-mononitrate (ISMN) is one of the most frequently used compounds in the treatment of coronary artery disease predominantly in the USA. However, ISMN was reported to induce endothelial dysfunction, which was corrected by vitamin C pointing to a crucial role of reactive oxygen species (ROS) in causing this phenomenon. We sought to elucidate the mechanism how ISMN causes endothelial dysfunction and oxidative stress in vascular tissue. Methods and results Male Wistar rats ( n = 69 in total) were treated with ISMN (75 mg/kg/day) or placebo for 7 days. Endothelin (ET) expression was determined by immunohistochemistry in aortic sections. Isosorbide-5-mononitrate infusion caused si…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIIsosorbide DinitratePharmacologymedicine.disease_causeBiochemistryMicechemistry.chemical_compoundSuperoxidesEnosInternal medicinePhysiology (medical)medicineAnimalsNitric Oxide DonorsEnzyme InhibitorsRats WistarEndothelial dysfunctionCyclic GMPAortaMice KnockoutNADPH oxidaseEndothelin-1biologybusiness.industryNADPH Oxidasesmedicine.diseasebiology.organism_classificationEndothelin 1BosentanRatsNitric oxide synthaseEndothelial stem cellOxidative StressNG-Nitroarginine Methyl EsterEndocrinologychemistryApocyninbiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineEndothelin receptorbusinessOxidative stressSignal Transductionmedicine.drugFree Radical Biology and Medicine
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Resveratrol Reverses Endothelial Nitric-Oxide Synthase Uncoupling in Apolipoprotein E Knockout Mice

2010

A crucial cause of the decreased bioactivity of nitric oxide (NO) in cardiovascular diseases is the uncoupling of the endothelial NO synthase (eNOS) caused by the oxidative stress-mediated deficiency of the NOS cofactor tetrahydrobiopterin (BH(4)). The reversal of eNOS uncoupling might represent a novel therapeutic approach. The treatment of apolipoprotein E knockout (ApoE-KO) mice with resveratrol resulted in the up-regulation of superoxide dismutase (SOD) isoforms (SOD1-SOD3), glutathione peroxidase 1 (GPx1), and catalase and the down-regulation of NADPH oxidases NOX2 and NOX4 in the hearts of ApoE-KO mice. This was associated with reductions in superoxide, 3-nitrotyrosine, and malondiald…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIISOD3SOD2ResveratrolAntioxidantsSuperoxide dismutaseMicechemistry.chemical_compoundApolipoproteins ESuperoxidesEnosMalondialdehydeInternal medicineStilbenesmedicineAnimalsGTP CyclohydrolaseMice KnockoutPharmacologychemistry.chemical_classificationReactive oxygen speciesbiologyReverse Transcriptase Polymerase Chain ReactionSuperoxide DismutaseChemistrySuperoxideMyocardiumTetrahydrobiopterinbiology.organism_classificationBiopterinIsoenzymesOxidative StressEndocrinologyBiochemistryResveratrolbiology.proteinRNATyrosineMolecular Medicinemedicine.drugJournal of Pharmacology and Experimental Therapeutics
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Acute ammonia intoxication induces an NMDA receptor-mediated increase in poly(ADP-ribose) polymerase level and NAD+ metabolism in nuclei of rat brain…

2004

Acute ammonia toxicity is mediated by excessive activation of NMDA receptors. Activation of NMDA receptors leads to activation of poly(ADP-ribose) polymerase (PARP) which mediates NMDA excitotoxicity. PARP is activated following DNA damage and may lead to cell death via NAD+ and ATP depletion. The aim of the present work was to assess whether acute ammonia intoxication in vivo leads to increased PARP in brain cells nuclei and to altered NAD+ and superoxide metabolism and the contribution of NMDA receptors to these alterations. Acute ammonia intoxication increases PARP content twofold in brain cells nuclei.NAD+ content decreased by 55% in rats injected with ammonia. This was not due to decre…

Malemedicine.medical_specialtyPoly ADP ribose polymeraseExcitotoxicityBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundNAD+ NucleosidaseAmide SynthasesAmmoniaSuperoxidesInternal medicinemedicineAnimalsNeurotoxinRats WistarReceptorBrain ChemistryCell NucleusProtein Synthesis InhibitorsSuperoxideNAD+ ADP-RibosyltransferaseBrainProteinsNADMolecular biologyRatsEndocrinologychemistryTyrosineNMDA receptorNAD+ kinasePoly(ADP-ribose) PolymerasesJournal of Neurochemistry
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Differential effects of diabetes on the expression of the gp91phox homologues nox1 and nox4.

2004

The nox2-dependent NADPH oxidase was shown to be a major superoxide source in vascular disease, including diabetes. Smooth muscle cells of large arteries lack the phagocytic gp91phox subunit of the enzyme; however, two homologues have been identified in these cells, nox1 and nox4. It remained to be established whether also increases in protein levels of the nonphagocytic NADPH oxidase contribute to increased superoxide formation in diabetic vessels. To investigate changes in the expression of these homologues, we measured their expression in aortic vessels of type I diabetic rats. Eight weeks after streptozotocin treatment, we found a doubling in nox1 protein expression, while the expressio…

Malemedicine.medical_specialtyXanthine OxidaseVasodilator AgentsBlotting WesternFluorescent Antibody TechniqueNitric OxideBiochemistryNitric oxideDiabetes Mellitus Experimentalchemistry.chemical_compoundNitroglycerinSuperoxidesPhysiology (medical)Internal medicinemedicineAnimalsNADH NADPH OxidoreductasesRats WistarXanthine oxidaseAortaNADPH oxidasebiologySuperoxideMyocardiumMicrofilament ProteinsElectron Spin Resonance SpectroscopyNOX4NADPH Oxidase 1Endothelial CellsNADPH OxidasesPhosphoproteinsImmunohistochemistryAcetylcholineRatsNitric oxide synthaseEndocrinologychemistryNADPH Oxidase 4NOX1cardiovascular systembiology.proteinNADPH Oxidase 1Nitric Oxide SynthaseCell Adhesion MoleculesFree radical biologymedicine
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Nebivolol inhibits superoxide formation by NADPH oxidase and endothelial dysfunction in angiotensin II-treated rats.

2006

Nebivolol is a β 1 -receptor antagonist with vasodilator and antioxidant properties. Because the vascular NADPH oxidase is an important superoxide source, we studied the effect of nebivolol on endothelial function and NADPH oxidase activity and expression in the well-characterized model of angiotensin II–induced hypertension. Angiotensin II infusion (1 mg/kg per day for 7 days) caused endothelial dysfunction in male Wistar rats and increased vascular superoxide as detected by lucigenin-derived chemiluminescence, as well as dihydroethidine staining. Vascular NADPH oxidase activity, as well as expression at the mRNA and protein level, were markedly upregulated, as well as NOS III uncoupled, …

Malerac1 GTP-Binding Proteinmedicine.medical_specialtyLuminescenceEndotheliumNitric Oxide Synthase Type IIIAdrenergic beta-AntagonistsNitric OxideFluorescenceCell LineNebivololchemistry.chemical_compoundHemoglobinsSuperoxidesInternal medicineInternal MedicinemedicineAnimalsHumansBenzopyransRats WistarCyclic GMPNitritesOxidase testNADPH oxidaseLuminescent AgentsbiologyChemistrySuperoxideAngiotensin IIMyocardiumNADPH OxidasesDicarbethoxydihydrocollidinePhosphoproteinsAngiotensin IINebivololRatsNitric oxide synthasemedicine.anatomical_structureEndocrinologyEthanolaminesNOX1biology.proteinAcridinesBlood VesselsLuminolEndothelium Vascularmedicine.drugSignal TransductionHypertension (Dallas, Tex. : 1979)
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