Search results for "Acyl-CoA Oxidase"

showing 10 items of 28 documents

The Inflammatory Response in Acyl-CoA Oxidase 1 Deficiency (Pseudoneonatal Adrenoleukodystrophy)

2012

Among several peroxisomal neurodegenerative disorders, the pseudoneonatal adrenoleukodystrophy (P-NALD) is characterized by the acyl-coenzyme A oxidase 1 (ACOX1) deficiency, which leads to the accumulation of very-long-chain fatty acids ( VLCFA) and inflammatory demyelination. However, the components of this inflammatory process in P-NALD remain elusive. In this study, we used transcriptomic profiling and PCR array analyses to explore inflammatory gene expression in patient fibroblasts. Our results show the activation of IL-1 inflammatory pathway accompanied by the increased secretion of two IL-1 target genes, IL-6 and IL-8 cytokines. Human fibroblasts exposed to very-long-chain fatty acids…

MESH: Inflammationperoxisomal disordersMESH: Osteopontinmedicine.medical_treatmentMESH : ImmunohistochemistryMESH : Transcriptomechemokine receptorsVoeding Metabolisme en Genomica0302 clinical medicineEndocrinologyMESH: Reverse Transcriptase Polymerase Chain ReactionAcyl-CoA oxidasemultiple-sclerosis lesionsMESH : OsteopontinMESH : Fatty AcidsCells CulturedOligonucleotide Array Sequence Analysis[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism0303 health sciencesOxidase testMESH : Gene Expression RegulationReverse Transcriptase Polymerase Chain ReactionFatty AcidsMESH: Acyl-CoA OxidaseMESH : Reverse Transcriptase Polymerase Chain ReactionPeroxisome[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismImmunohistochemistryMESH: Gene Expression RegulationMetabolism and Genomics3. Good healthMESH: Fatty AcidsMESH : Oligonucleotide Array Sequence AnalysisCytokineMetabolisme en GenomicaACOX1AdrenoleukodystrophyNutrition Metabolism and GenomicsMESH : Acyl-CoA Oxidasemedicine.symptomInflammation MediatorsMESH: Cells Culturedmedicine.medical_specialtyMESH : Interleukin-8MESH : Interleukin-6MESH: Inflammation MediatorsInflammationBiologyin-vitroMESH : Interleukin-1MESH : Inflammation Mediators03 medical and health sciencesVoedingInternal medicinePeroxisomal disordernf-kappa-bMESH : Cells CulturedMESH : Fibroblastsmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologygene[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyNutrition030304 developmental biologyVLAGInflammationMESH: HumansMESH : InflammationInterleukin-6MESH: TranscriptomeInterleukin-8MESH : HumansMESH: Interleukin-1MESH: ImmunohistochemistryFibroblastsmedicine.diseaseMESH: Interleukin-6MESH: Interleukin-8EndocrinologyGene Expression RegulationMESH: FibroblastsMESH: Oligonucleotide Array Sequence AnalysiscellsBrief ReportsOsteopontinmicroarray analysisAcyl-CoA OxidaseTranscriptomeinterleukin-1030217 neurology & neurosurgeryx-linked adrenoleukodystrophyInterleukin-1
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Peroxisomal beta-oxidation activities and gamma-decalactone production by the yeast Yarrowia lipolytica.

1998

International audience; gamma-Decalactone is a peachy aroma compound resulting from the peroxisomal beta-oxidation of ricinoleic acid by yeasts. The expression levels of acyl-CoA oxidase (gene deletion) and 3-ketoacyl-CoA thiolase activities (gene amplification on replicative plasmids) were modified in the yeast Yarrowia lipolytica. The effects of these modifications on beta-oxidation were measured. Overexpression of thiolase activity did not have any effect on the overall beta-oxidation activity. The disruption of one of the acyl-CoA oxidase genes resulted in an enhanced activity. The enhancement led to an increase of overall beta-oxidation activity but reduced the gamma-decalactone produc…

MESH: Oxidation-ReductionRicinoleic acidMESH: MicrobodiesMicrobodiesApplied Microbiology and BiotechnologyAROME DE PECHELactoneschemistry.chemical_compoundMESH : BiotransformationYeastsMESH : Microbodies[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAcyl-CoA oxidaseMESH: Blotting NorthernNorthern[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[INFO.INFO-BT]Computer Science [cs]/Biotechnology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyBiotransformationMESH : Oxidation-ReductionMESH: BiotransformationMESH : YeastsOxidase testbiologyBlottingCatabolismThiolaseMESH: YeastsMESH : Blotting NorthernYarrowiaGeneral MedicinePeroxisomeBlotting Northernbiology.organism_classificationYeastMESH : LactonesMESH: Ricinoleic Acids[SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology[INFO.INFO-BT] Computer Science [cs]/BiotechnologyBiochemistrychemistryMESH : Ricinoleic AcidsACYL COA OXYDASERicinoleic AcidsOxidation-Reduction[ INFO.INFO-BT ] Computer Science [cs]/BiotechnologyMESH: LactonesBiotechnology
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A human relevance investigation of PPARα-mediated key events in the hepatocarcinogenic mode of action of propaquizafop in rats

2018

Propaquizafop is an herbicide with demonstrated hepatocarcinogenic activity in rodents. A rodent-specific mode of action (MOA) in the liver via activation of peroxisome proliferator-activated receptor α (PPARα) has been postulated based on existing data. Experience with PPARα-inducing pharmaceuticals indicates a lack of human relevance of this MOA. The objective of the present investigation was to evaluate the dependency of early key events leading to liver tumors on PPARα activation in wildtype (WT) compared to PPARα-knockout (KO) rats following 2 weeks exposure to 75, 500 and 1000 ppm propaquizafop in the diet. In WT rats, both WY-14643 (50 mg/kg bw/day) and propaquizafop (dose-dependentl…

Male0301 basic medicinemedicine.medical_specialtyPeroxisome proliferator-activated receptor010501 environmental sciencesBiologyToxicologyRisk Assessment01 natural sciencesMuscle hypertrophyRats Sprague-Dawley03 medical and health sciencesCytochrome P-450 Enzyme SystemInternal medicinemedicineAnimalsHumansAcyl-CoA oxidasePPAR alphaRelevance (information retrieval)Enzyme inducerReceptorMode of actionCarcinogen0105 earth and related environmental scienceschemistry.chemical_classificationGlutathione PeroxidaseHerbicidesGlutathione peroxidaseLiver NeoplasmsOrgan SizeGeneral MedicineGlutathioneDiet030104 developmental biologyEndocrinologyLiverchemistrybiology.proteinKey (cryptography)Acyl-CoA OxidasePropionatesRats TransgenicNeuroscienceToxicology Letters
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A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver.: ThB …

2011

International audience; Peroxisomal 3-ketoacyl-CoA thiolase B (Thb) catalyzes the final step in the peroxisomal β-oxidation of straight-chain acyl-CoAs and is under the transcription control of the nuclear hormone receptor PPARα. PPARα binds to and is activated by the synthetic compound Wy14,643 (Wy). Here, we show that the magnitude of Wy-mediated induction of peroxisomal β-oxidation of radiolabeled (1-(14)C) palmitate was significantly reduced in mice deficient for Thb. In contrast, mitochondrial β-oxidation was unaltered in Thb(-/-) mice. Given that Wy-treatment induced Acox1 and MFP-1/-2 activity at a similar level in both genotypes, we concluded that the thiolase step alone was respons…

MaleMESH: HepatomegalyPalmitatesMESH : PyrimidinesMESH : Gene DeletionBiochemistryelement-binding proteinsMESH : Acetyl-CoA C-AcyltransferaseMiceMESH: Up-RegulationMESH: AnimalsMESH : Up-RegulationMESH: Lipid Metabolism0303 health sciencesMESH : Gene Expression RegulationThiolase030302 biochemistry & molecular biologyGeneral MedicineMESH : HepatomegalyUp-Regulationzellweger-syndromePeroxisome ProliferatorsMESH: Peroxisome ProliferatorsHepatomegalySterol Regulatory Element Binding Protein 2peroxisomal 3-ketoacyl-CoA thiolase BMESH: Mitochondria3-oxoacyl-coa thiolaseLathosterolfatty-acid oxidationrat-liverMESH: Sterol Regulatory Element Binding Protein 203 medical and health sciencesMESH : Sterol Regulatory Element Binding Protein 2HumansPPAR alphaMESH : Peroxisome Proliferators[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPPARaVLAGMESH : Oxidation-ReductionFatty Acid Oxidation.MESH: HumansCholesterolMESH : HumanscholesterolLipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinchemistryMESH: PyrimidinesCholesterol; Micro-array analysis; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα and SREBP-2; Wy14643Fatty Acid OxidationGene DeletionMESH: LiverMESH: Oxidation-ReductionMESH: Signal TransductionMESH: Mice KnockoutVoeding Metabolisme en Genomicachemistry.chemical_compoundMESH: CholesterolMESH : Lipid MetabolismWy14MESH : PalmitatesMESH: PPAR alphaMESH : CholesterolMice Knockoutneuronal migration643PeroxisomeAcetyl-CoA C-AcyltransferaseMESH: Gene Expression RegulationMetabolism and GenomicsMitochondriaLiverBiochemistryMicro-array analysisMetabolisme en GenomicaACOX1Nutrition Metabolism and GenomicsMESH : MitochondriaOxidation-ReductionSignal Transductionacyl-coa oxidasecholesterol-synthesisMESH : MaleMESH : PPAR alphaPeroxisome ProliferationPPARα and SREBP-2Biologybeta-oxidationVoedingproliferator-activated receptorsMESH : MicePeroxisomesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Mice030304 developmental biologySCP2NutritionMESH : Signal TransductionMESH : LiverMESH: PalmitatesMESH: MalePyrimidinesMESH: Acetyl-CoA C-AcyltransferaseGene Expression RegulationMESH: Gene DeletionMESH : Mice KnockoutMESH : AnimalsMESH : Peroxisomes
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Dehydroepiandrosterone up-regulates the Adrenoleukodystrophy-related gene (ABCD2) independently of PPAR alpha in rodents

2007

International audience; X-linked adrenoleukodystrophy (X-ALD) is a neurodegenerative disease caused by mutations in the ABCD1 gene, which encodes a peroxisomal ABC transporter, ALDP, supposed to participate in the transport of very long chain fatty acids (VLCFA). The adrenoleukodystrophyrelated protein (ALDRP), which is encoded by the ABCD2 gene, is the closest homolog of ALDP and is considered as a potential therapeutic target since functional redundancy has been demonstrated between the two proteins. Pharmacological induction of Abcd2 by fibrates through the activation of PPARa has been demonstrated in rodent liver. DHEA, the most abundant steroid in human, is described as a PPARa activat…

MalePEROXISOMEProhormonePeroxisome proliferator-activated receptorATP-binding cassette transporterBiochemistryMice0302 clinical medicineABC TRANSPORTERSPPAR-ALPHAAdrenal GlandsTestisDHEACells Culturedchemistry.chemical_classification0303 health sciencesSex CharacteristicsbiologyBrainGeneral MedicineOrgan SizePeroxisome3. Good healthUp-RegulationLiverAdrenoleukodystrophyFemalemedicine.drugAndrostenediolmedicine.medical_specialtyADRENOLEUKODYSTROPHYATP Binding Cassette Transporter Subfamily D03 medical and health sciencesABCD3Internal medicinemedicineABCD2AnimalsPPAR alpha[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRats Wistar030304 developmental biologyActivator (genetics)Body Weightnutritional and metabolic diseasesMembrane ProteinsDehydroepiandrosteronemedicine.diseaseRatsMice Inbred C57BLEndocrinologychemistrybiology.proteinHepatocytesATP-Binding Cassette TransportersAcyl-CoA Oxidase030217 neurology & neurosurgery
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Differential proto-oncogene mRNA induction from rats treated with peroxisome proliferators

1990

After experimental treatment of rats with clofibrate or ciprofibrate, two peroxisomes proliferators with hypolipidemic activity, RNAs were prepared from liver, kidney, heart and brain; hybridization was done with DNA probes for c-myc and c-Ha-ras oncogenes and for cyanide insensitive Acyl CoA oxidase, a peroxisomal protein. c-myc mRNA is highly abundant in liver and at a lower extent in kidney, especially after treatment with ciprofibrate; clofibrate also allows a c-myc mRNA increase, but at a lower extent. c-Ha-ras, which is already expressed in all tested tissues from control animals, is stimulated by clofibrate and ciprofibrate treatments. Comparatively these compounds stimulate the cyan…

MaleSomatic cellGenes mycBiophysicsBiologyKidneyMicrobodiesBiochemistryClofibric AcidProto-OncogenesmedicineAnimalsAcyl-CoA oxidaseClofibrateRNA MessengerMolecular BiologyHypolipidemic AgentsKidneyMessenger RNAClofibrateOncogeneFibric AcidsCell BiologyPeroxisomeMolecular biologyRats Inbred F344RatsGenes rasmedicine.anatomical_structureGene Expression RegulationLiverOrgan SpecificityAcyl-CoA OxidaseCiprofibrateOxidoreductasesmedicine.drugBiochemical and Biophysical Research Communications
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Changes of peroxisomal fatty acid metabolism during cold acclimatization in hibernating jerboa (Jaculus orientalis)

2003

Abstract Jerboa (Jaculus orientalis) is a deep hibernator originating from sub-desert highlands and represents an excellent model to help to understand the incidence of seasonal variations of food intake and of body as well as environmental temperatures on lipid metabolism. In jerboa, hibernation processes are characterized by changes in the size of mitochondria, the number of peroxisomes in liver and in the expression of enzymes linked to fatty acid metabolism. In liver and kidney, cold acclimatization shows an opposite effect on the activities of the mitochondrial acyl-CoA dehydrogenase (–50%) and the peroxisomal acyl-CoA oxidase (AOX) (+50%), while in brown and white adipose tissues, bot…

Malemedicine.medical_specialtyAcclimatizationAdipose tissueRodentiaWhite adipose tissueBiologyFatty acid degradationBiochemistryAcclimatizationchemistry.chemical_compoundHibernationInternal medicineBrown adipose tissuePeroxisomesmedicineAnimalsRNA MessengerFatty acid metabolismFatty AcidsLipid metabolismGeneral MedicinePeroxisomeMitochondriaCold TemperatureEnzyme ActivationEndocrinologymedicine.anatomical_structureLiverchemistryBiochemistryAcyl-CoA OxidaseBody Temperature RegulationBiochimie
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Difference between Guinea Pig and Rat in the Liver Peroxisomal Response to Equivalent Plasmatic Level of Ciprofibrate

1996

Abstract Guinea pig was previously classified as a species nonresponsive to peroxisome proliferators. However, none of the previous reports was based on pharmacokinetic data. Here, after a comparative pharmacokinetic study between guinea pig and rat, we evaluate the guinea pig liver peroxisomal response to ciprofibrate, a hypolipemic agent and a potent peroxisome proliferator in rat. (1) Pharmacokinetic results show that plasmatic concentrations of ciprofibrate are equivalent in guinea pig and rat when guinea pigs are treated with ciprofibrate at 30 mg/kg twice a day and rats are treated at 3 mg/kg once a day. (2) The treatment of guinea pigs at 30 mg/kg twice a day for 2 weeks leads to a s…

Malemedicine.medical_specialtyGuinea PigsBiophysicsGene ExpressionPeroxisome ProliferationBiologyCell FractionationMicrobodiesBiochemistryMixed Function OxygenasesGuinea pigClofibric AcidCytochrome P-450 Enzyme SystemSpecies SpecificityPharmacokineticsInternal medicinemedicineAnimalsRNA MessengerMolecular BiologyHypolipidemic AgentsMessenger RNAOxidase testFibric AcidsPeroxisomeBlotting NorthernRatsEndocrinologyLiverMicrosomeAcyl-CoA OxidaseCiprofibrateCytochrome P-450 CYP4ADNA ProbesOxidoreductasesmedicine.drugArchives of Biochemistry and Biophysics
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Delayed effects of ciprofibrate on rat liver peroxisomal properties and proto-oncogene expression.

1995

Peroxisome proliferators (PPs) are non-genotoxic carcinogens in rodents. Their reversible effects on rat liver have been studied with ciprofibrate and fenofibrate. We found that with the hypolipemic drug fenofibrate a pause of 28 days is sufficient for a return to normal status, whereas with the highly potent PP ciprofibrate, the stimulation of ACO mRNA levels remains after its withdrawal. We investigated the effects of the renewal of the treatment with PPs on other peroxisomal parameters and proto-oncogene expression using Wistar rats. Interestingly, c-myc expression was enhanced even upon drug withdrawal, and was more stimulated by the second exposure to ciprofibrate, while c-fos expressi…

Malemedicine.medical_specialtyTime FactorseducationStimulationMitochondria LiverBiologyBiochemistryMicrobodiesDrug withdrawalClofibric AcidFenofibrateInternal medicineProto-Oncogene ProteinsGene expressionmedicineAnimalsRats WistarCarcinogenPharmacologyFenofibrateOncogeneFibric AcidsPeroxisomemedicine.diseaseRatsEndocrinologyLiverMicrosomes LiverCiprofibrateAcyl-CoA OxidaseOxidoreductasesmedicine.drugBiochemical pharmacology
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Phosphorylation of peroxisome proliferator-activated receptor α in rat Fao cells and stimulation by ciprofibrate

1999

The basic mechanism(s) by which peroxisome proliferators activate peroxisome proliferator-activated receptors (PPARs) is (are) not yet fully understood. Given the diversity of peroxisome proliferators, several hypotheses of activation have been proposed. Among them is the notion that peroxisome proliferators could activate PPARs by changing their phosphorylation status. In fact, it is well known that several members of the nuclear hormone receptor superfamily are regulated by phosphorylation. In this report, we show that the rat Fao hepatic-derived cell line, known to respond to peroxisome proliferators, exhibited a high content of PPARalpha. Alkaline phosphatase treatment of Fao cell lysat…

Peroxisome proliferator-activated receptor gammaPhosphataseReceptors Cytoplasmic and NuclearPeroxisome proliferator-activated receptorBiologyMicrobodiesBiochemistryCell LineClofibric AcidmedicineAnimalsEnzyme InhibitorsPhosphorylationPharmacologychemistry.chemical_classificationFibric Acidsfood and beveragesPeroxisomePhosphoric Monoester HydrolasesRatsGene Expression RegulationBiochemistryNuclear receptorchemistryPhosphorylationPeroxisome Proliferatorslipids (amino acids peptides and proteins)Acyl-CoA OxidasePeroxisome proliferator-activated receptor alphaCiprofibrateOxidoreductasesTranscription Factorsmedicine.drugBiochemical Pharmacology
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