Search results for "glutamate-cysteine ligase"

showing 10 items of 10 documents

Glutathione deficiency of the Arabidopsis mutant pad2-1 affects oxidative stress-related events, defense gene expression and hypersensitive response

2011

L'article original est publié par The American Society of Plant Biologists; International audience; The Arabidopsis (Arabidopsis thaliana) phytoalexin-deficient mutant pad2-1 displays enhanced susceptibility to a broad range of pathogens and herbivorous insects that correlates with deficiencies in the production of camalexin, indole glucosinolates, and salicylic acid (SA). The pad2-1 mutation is localized in the GLUTAMATE-CYSTEINE LIGASE (GCL) gene encoding the first enzyme of glutathione biosynthesis. While pad2-1 glutathione deficiency is not caused by a decrease in GCL transcripts, analysis of GCL protein level revealed that pad2-1 plants contained only 48% of the wild-type protein amoun…

0106 biological sciencesPhysiologyMutantGlutathione reductaseArabidopsisOligosaccharidesPlant Science01 natural scienceschemistry.chemical_compoundAnti-Infective AgentsGene Expression Regulation PlantCamalexinArabidopsis thaliana0303 health sciencesGlutathioneBiochemistryHost-Pathogen InteractionsDisease SusceptibilitySalicylic AcidOxidation-ReductionSignal TransductionHypersensitive responsePhytophthoradisease resistanceBiologyNitric Oxiderespiratory burst oxidase homolog d[SDV.GEN.GPL]Life Sciences [q-bio]/Genetics/Plants genetics03 medical and health sciencesStress PhysiologicalGeneticsPlants Interacting with Other Organismsglutathione reductase030304 developmental biologyPlant DiseasesArabidopsis ProteinsCell MembraneWild typeGlutathioneHydrogen Peroxidebiology.organism_classificationMolecular biologyPlant LeavesOxidative StresschemistryMutationglutathione-s-transferaseIsochorismate synthasebiology.proteinglutamate-cysteine ligaseReactive Oxygen Species010606 plant biology & botany
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Chronic aspartame intake causes changes in the trans-sulphuration pathway, glutathione depletion and liver damage in mice

2017

No-caloric sweeteners, such as aspartame, are widely used in various food and beverages to prevent the increasing rates of obesity and diabetes mellitus, acting as tools in helping control caloric intake. Aspartame is metabolized to phenylalanine, aspartic acid, and methanol. Our aim was to study the effect of chronic administration of aspartame on glutathione redox status and on the trans-sulphuration pathway in mouse liver. Mice were divided into three groups: control; treated daily with aspartame for 90 days; and treated with aspartame plus N-acetylcysteine (NAC). Chronic administration of aspartame increased plasma alanine aminotransferase (ALT) and aspartate aminotransferase activities…

0301 basic medicinemedicine.medical_specialtyGlutamate-Cysteine LigaseClinical BiochemistryPhenylalanineBiochemistryMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineAspartic acidmedicineAnimalsHumansCysteineAspartamelcsh:QH301-705.5lcsh:R5-920S-adenosylmethionineMethioninebiologyAspartameChemistryOrganic ChemistryCystathionine gamma-LyaseMethionine AdenosyltransferaseGlutathioneGlutathioneCystathionine beta synthaseN-acetylcysteineAcetylcysteine030104 developmental biologyEndocrinologyGCLCGene Expression RegulationLiverlcsh:Biology (General)BiochemistrySweetening Agents030220 oncology & carcinogenesisbiology.proteinChemical and Drug Induced Liver Injurylcsh:Medicine (General)Research PaperCysteineRedox Biology
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Enhanced reduction in oxidative stress and altered glutathione and thioredoxin system response to unsaturated fatty acid load in familial hypercholes…

2014

Abstract Objectives Familial hypercholesterolemia (FH) is characterized by increased oxidative stress (OS) levels. In the postprandial state, lipids and lipoproteins modulate OS status through their impact on pro-oxidant and antioxidant mechanisms. The objective of this study was to evaluate in patients with FH the response to an unsaturated oral fat load test (OFLT) by analyzing the mRNA levels of genes involved in the glutathione and thioredoxin antioxidant systems. Design and Methods We analyzed 14 FH patients and 20 normolipidemic and normoglycemic controls. In both groups, mRNA values of antioxidant enzyme genes (glutathione and thioredoxin systems) were determined at baseline and at 2…

AdultMalemedicine.medical_specialtyGPX1Antioxidantmedicine.medical_treatmentGlutamate-Cysteine LigaseClinical Biochemistrymedicine.disease_causeGPX4Gene Expression Regulation EnzymologicGlutathione SynthaseHyperlipoproteinemia Type IIchemistry.chemical_compoundThioredoxinsDietary Fats UnsaturatedInternal medicinemedicineHumansUnsaturated fatty acidGlutathione PeroxidaseChemistryReverse Transcriptase Polymerase Chain ReactionGeneral MedicineGlutathioneFastingMiddle AgedPhospholipid Hydroperoxide Glutathione PeroxidaseGlutathioneOxidative StressPostprandialEndocrinologyGlutathione ReductaseFemaleThioredoxinOxidation-ReductionOxidative stressClinical biochemistry
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Elimination of Ehrlich tumours by ATP-induced growth inhibition, glutathione depletion and X-rays

1995

ATP-induced tumour growth inhibition is accompanied by a selective decrease in the content of the tripeptide glutathione (GSH) within the cancer cells in vivo. Depletion of cellular GSH sensitizes tumours to chemotherapy and radiation, but the usefulness of this depletion depends on whether the levels of GSH can be reduced in the tumour relative to normal tissues. We report here that administration of ATP in combination with diethylmaleate and X-rays leads to complete regression of 95% of Ehrlich ascites tumours in mice. This shows that an aggressive tumour can be eliminated by using a therapy based on modulation of GSH levels in cancer cells.

MaleRadiation-Sensitizing AgentsGlutamate-Cysteine Ligasemedicine.medical_treatmentAntineoplastic AgentsTripeptideBiologyGeneral Biochemistry Genetics and Molecular BiologyMicechemistry.chemical_compoundAdenosine TriphosphateIn vivoMethionine SulfoximinemedicineAnimalsButhionine sulfoximineEnzyme InhibitorsCarcinoma Ehrlich TumorButhionine SulfoximineChemotherapyX-RaysMaleatesGeneral MedicineGlutathioneHydrogen-Ion ConcentrationCombined Modality TherapyGlutathionechemistryBiochemistryCancer cellCancer researchGrowth inhibitionAdenosine triphosphateCell DivisionNature Medicine
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Glutamate cysteine ligase up-regulation fails in necrotizing pancreatitis

2007

Glutathione depletion is a key factor in the development of acute pancreatitis. Our aim was to study the regulation of glutamate cysteine ligase, the rate-limiting enzyme in glutathione synthesis, in edematous or necrotizing pancreatitis in rats. Glutathione levels were kept low in necrotizing pancreatitis for several hours, with no increase in protein or mRNA levels of glutamate cysteine ligase subunits, despite binding of RNA polymerase II to their promoters and coding regions. The survival signal pathway mediated by ERK and c-MYC was activated, and c-MYC was recruited to the promoters. The failure in gene up-regulation seems to be due to a marked increase in cytosolic ribonuclease activi…

MaleTaurocholic AcidMAPK/ERK pathwayRNase PGlutamate-Cysteine LigaseRNA StabilityRNA polymerase IIBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundRibonucleasesTranscription (biology)Physiology (medical)medicineAnimalsEdemaRNA MessengerRibonucleaseRats WistarbiologyPancreatitis Acute NecrotizingNF-κBGlutathionemedicine.diseaseGlutathioneMolecular biologyRatsUp-RegulationPancreatitischemistrybiology.proteinPancreatitisRNA Polymerase IICeruletideTranscription FactorsFree Radical Biology and Medicine
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Glucocorticoid receptor knockdown decreases the antioxidant protection of B16 melanoma cells: an endocrine system-related mechanism that compromises …

2014

We previously reported an interorgan system in which stress-related hormones (corticosterone and noradrenaline), interleukin-6, and glutathione (GSH) coordinately regulate metastatic growth of highly aggressive B16-F10 melanoma cells. Corticosterone, at levels measured in tumor-bearing mice, also induces apoptotic cell death in metastatic cells with low GSH content. In the present study we explored the potential role of glucocorticoids in the regulation of metastatic cell death/survival during the early stages of organ invasion. Glucocorticoid receptor (GCR) knockdown decreased the expression and activity of γ-glutamylcysteine synthetase (γ-GCS), the rate-limiting step in GSH synthesis, in …

MaleTumor PhysiologyGlutathione reductaseCancer TreatmentMelanoma ExperimentalGene Expressionlcsh:MedicineBiochemistryAntioxidantsMetastasisAnalytical Chemistrychemistry.chemical_compoundOxidative DamageMiceGlucocorticoid receptorSpectrum Analysis TechniquesCell SignalingNeoplasmsMolecular Cell BiologyBasic Cancer ResearchMedicine and Health SciencesNeoplasm Metastasislcsh:Sciencechemistry.chemical_classificationMultidisciplinaryCell DeathGlutathione peroxidaseEndocrine TherapyFlow CytometryGlutathioneChemistrymedicine.anatomical_structureOncologyResearch DesignSpectrophotometryPhysical SciencesCytophotometryGlucocorticoidmedicine.drugResearch ArticleSignal Transductionmedicine.medical_specialtyEndotheliumClinical Research DesignCell SurvivalGlutamate-Cysteine LigaseDown-RegulationEndocrine SystemBiologyResearch and Analysis MethodsCell LineReceptors GlucocorticoidInternal medicineCell Line TumormedicineGeneticsAnimalsHumansAnimal Models of DiseaseOncogenic Signalinglcsh:RBiology and Life SciencesEndothelial CellsGlutathioneCell BiologyMice Inbred C57BLEndocrinologyHEK293 CellschemistryCell cultureCancer cellAnimal Studieslcsh:QEndothelium VascularCytometryPLoS ONE
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Vitamin E deficiency induces liver nuclear factor-κB DNA-binding activity and changes in related genes

2005

The biological functions of vitamin E have been classically attributed to its property as a potent inhibitor of lipid peroxidation in cellular membranes. However, in 1991, Azzi's group first described that alpha-tocopherol inhibits smooth muscle cell proliferation in a protein kinase C (PKC)-dependent way, demonstrating a non-antioxidant cell signalling function for vitamin E. More recently, the capacity of alpha-tocopherol to modulate gene expression with the implication of different transcription factors, beyond its antioxidant properties, has also been established. This study was to determine the effect of vitamin E-deficiency on liver nuclear factor-kappa B (NF-kappaB) DNA-binding activ…

MaleVitaminChromatin ImmunoprecipitationGlutamate-Cysteine Ligasemedicine.medical_treatmentBlotting WesternBiologyBiochemistrychemistry.chemical_compoundCyclin D1CyclinsMalondialdehydemedicineAnimalsVitamin EVitamin E DeficiencyRNA MessengerRats WistarTranscription factorVitamin EBody WeightNF-kappa BPromoterDNAGeneral MedicineCell cycleGlutathioneRatsCell biologyGene Expression RegulationLiverBiochemistrychemistryVitamin E deficiencyChromatin immunoprecipitationFree Radical Research
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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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Age-dependent changes in the transcription profile of long-lived Drosophila over-expressing glutamate cysteine ligase

2011

Abstract In our prior studies ( Orr et al., 2005 ) we achieved a 30–50% increase in the life span of Drosophila by manipulating glutathione (GSH) production in neuronal tissues, through over-expression of glutamate-cysteine ligase (GCL), a key enzyme in glutathione biosynthesis. In the present study, we identified gene response patterns from which plausible mechanisms responsible for the observed effects on life span might be inferred. Functional clustering analysis of the transcriptome data revealed that biological processes affected by GCLc in young flies (10 days) were generally related to cell morphogenesis and differentiation, while those in older flies were associated with nucleosome …

Nucleosome organizationAgingGlutamate-Cysteine LigaseLongevityBiologyTranscriptomechemistry.chemical_compoundTranscription (biology)MorphogenesisAnimalsGeneOligonucleotide Array Sequence AnalysisGeneticschemistry.chemical_classificationDNA ligaseCell morphogenesisGene Expression ProfilingfungiCell DifferentiationGlutathioneGlutathioneImmunity HumoralNucleosomesDrosophila melanogasterGCLCchemistryDevelopmental BiologyMechanisms of Ageing and Development
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Age-dependent regulation of antioxidant genes by p38α MAPK in the liver

2018

p38α is a redox sensitive MAPK activated by pro-inflammatory cytokines and environmental, genotoxic and endoplasmic reticulum stresses. The aim of this work was to assess whether p38α controls the antioxidant defense in the liver, and if so, to elucidate the mechanism(s) involved and the age-related changes. For this purpose, we used liver-specific p38α-deficient mice at two different ages: young-mice (4 months-old) and old-mice (24 months-old). The liver of young p38α knock-out mice exhibited a decrease in GSH levels and an increase in GSSG/GSH ratio and malondialdehyde levels. However, old mice deficient in p38α had higher hepatic GSH levels and lower GSSG/GSH ratio than young p38α knock-…

ROS Reactive oxygen species;RSK1 Ribosomal S6 kinase10301 basic medicineMAPK/ERK pathwayAgingHPLC High-performance liquid chromatographyAntioxidantmedicine.medical_treatmentTBP TATA-binding proteinClinical BiochemistryDEN Diethyl nitrosamine;MKP-1 MAPK phosphatase-1IκB kinaseGCLc Glutamate cysteine ligase catalytic subunitp38 Mitogen-Activated Protein KinasesG6PDH Glucose-6-phosphate dehydrogenaseBiochemistryAntioxidantsMicechemistry.chemical_compoundSuperoxide Dismutase-1Akt Protein kinase B0302 clinical medicineNrf2 Nuclear factor erythroid 2-related factor-2IL InterleukinSOD1 Cu/Zn-superoxide dismutaselcsh:QH301-705.5Mice KnockoutMK2 MAP-activated protein kinase 2;PGC-1α Peroxisome proliferator-activated receptor gamma coactivator 1-alphachemistry.chemical_classificationlcsh:R5-920Trx ThioredoxinGlutathione DisulfideTNF-α Tumor necrosis factor-alphabiologyLPS Lipopolysaccharide;GSSG Oxidized glutathione;MEF Mouse embryonic fibroblastsNF-kappa BGstm1 Glutathione S-transferase mu 1CatalaseEndoplasmic Reticulum StressGlutathioneLiverGSH Reduced glutathione;Catalase030220 oncology & carcinogenesisJNK c-Jun N-terminal kinaselcsh:Medicine (General)Research Papermedicine.medical_specialtyNF-E2-Related Factor 2Glutamate-Cysteine LigaseMKK MAPK kinaseAP-1 Activator protein-1IKK IƙB KinaseGene Expression Regulation EnzymologicSuperoxide dismutase03 medical and health sciencesInternal medicineGlutamate cysteine ligaseEGFR Epidermal growth factor receptormedicineAnimalsNuclear factor ƙBAnd catalaseChIP Chromatin immunoprecipitation;Protein kinase BNF-ƙB Nuclear factor kappa BSuperoxide DismutaseSuperoxide dismutase 1Superoxide dismutase 2Organic ChemistryGlutathioneASK1 Apoptosis signal-regulating kinase 1ATF2 activating transcription factor 2;030104 developmental biologyEndocrinologyEnzymeHsp Heat shock proteinlcsh:Biology (General)chemistrybiology.proteinSOD2 Mn-superoxide dismutaseMAPK mitogen activated protein kinaseNEM N-ethyl maleimide;Redox Biology
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