Search results for "acids"

showing 10 items of 3520 documents

Lipids Nutrients in Parkinson and Alzheimer’s Diseases: Cell Death and Cytoprotection

2020

Neurodegenerative diseases, particularly Parkinson’s and Alzheimer’s, have common features: protein accumulation, cell death with mitochondrial involvement and oxidative stress. Patients are treated to cure the symptoms, but the treatments do not target the causes; so, the disease is not stopped. It is interesting to look at the side of nutrition which could help prevent the first signs of the disease or slow its progression in addition to existing therapeutic strategies. Lipids, whether in the form of vegetable or animal oils or in the form of fatty acids, could be incorporated into diets with the aim of preventing neurodegenerative diseases. These different lipids can inhibit the cytotoxi…

Programmed cell deathParkinson's diseaseInflammationReviewDiseasePharmacologyMitochondrionmedicine.disease_causelipids nutrientsCatalysislcsh:ChemistryInorganic ChemistrysynucleinFish OilsAlzheimer DiseaseHumansPlant OilsMedicinePhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopybusiness.industryFatty AcidsOrganic ChemistryapoptosisamyloidParkinson DiseaseNutrientsGeneral Medicinemedicine.diseaseLipidsCytoprotectionComputer Science ApplicationsmitochondriaOxidative Stresslcsh:Biology (General)lcsh:QD1-999CytoprotectionParkinson’s diseaseSynucleinTaumedicine.symptombusinessAlzheimer’s diseaseOxidative stressInternational Journal of Molecular Sciences
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Lovastatin attenuates ionizing radiation-induced normal tissue damage in vivo.

2009

Abstract Background and purpose HMG-CoA-reductase inhibitors (statins) are widely used lipid-lowering drugs. Moreover, they have pleiotropic effects on cellular stress responses, proliferation and apoptosis in vitro . Here, we investigated whether lovastatin attenuates acute and subchronic ionizing radiation-induced normal tissue toxicity in vivo . Materials and methods Four hours to 24h after total body irradiation (6Gy) of Balb/c mice, acute pro-inflammatory and pro-fibrotic responses were analyzed. To comprise subchronic radiation toxicity, mice were irradiated twice with 2.5Gy and analyses were performed 3weeks after the first radiation treatment. Molecular markers of inflammation and f…

Programmed cell deathPathologymedicine.medical_specialtyStatinmedicine.drug_classCell SurvivalPharmacologyRadiation DosageMiceRandom AllocationIn vivoFibrosisReference ValuesRadiation IonizingmedicineAnimalsHumansRadiology Nuclear Medicine and imagingLovastatinRNA MessengerRadiation InjuriesLungProbabilityMice Inbred BALB CChemistryTumor Necrosis Factor-alphaNF-kappa BDose-Response Relationship RadiationHematologymedicine.diseaseCTGFIntestinesDisease Models AnimalRadiation Injuries ExperimentalOncologyLiverApoptosisToxicitylipids (amino acids peptides and proteins)FemaleLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsInflammation Mediatorsmedicine.drugDNA DamageRadiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
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Side effects of oxysterols: cytotoxicity, oxidation, inflammation, and phospholipidosis.

2008

Oxysterols are 27-carbon atom molecules resulting from autoxidation or enzymatic oxidation of cholesterol. They are present in numerous foodstuffs and have been demonstrated to be present at increased levels in the plasma of patients with cardiovascular diseases and in atherosclerotic lesions. Thus, their role in lipid disorders is widely suspected, and they might also be involved in important degenerative diseases such as Alzheimer's disease, osteoporosis, and age-related macular degeneration. Since atherosclerosis is associated with the presence of apoptotic cells and with oxidative and inflammatory processes, the ability of some oxysterols, especially 7-ketocholesterol and 7β-hydrox…

Programmed cell deathPhysiologyImmunologyBiophysicsInflammationApoptosisOxidative phosphorylationPharmacologyLipidosesBiochemistryPhospholipidosischemistry.chemical_compoundmedicinepolycyclic compoundsAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsCytotoxicitylcsh:QH301-705.5PhospholipidsPhospholipidosisInflammationlcsh:R5-920ChemistryCholesterolGeneral NeuroscienceCell BiologyGeneral MedicineOxysterolsAtherosclerosisHydroxycholesterolsBiochemistrylcsh:Biology (General)Apoptosislipids (amino acids peptides and proteins)medicine.symptomSignal transductionlcsh:Medicine (General)Oxidation-ReductionBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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Apoptosis: a relevant tool for anticancer therapy.

2006

Apoptosis is a form of cell death that permits the removal of damaged, senescent or unwanted cells in multicellular organisms, without damage to the cellular microenvironment. Defective apoptosis represents a major causative factor in the development and progression of cancer. The majority of chemotherapeutic agents, as well as radiation, utilize the apoptotic pathway to induce cancer cell death. Resistance to standard chemotherapeutic strategies also seems to be due to alterations in the apoptotic pathway of cancer cells. Recent knowledge on apoptosis has provided the basis for novel targeted therapies that exploit apoptosis to treat cancer. These new target include those acting in the ext…

Programmed cell deathSettore MED/06 - Oncologia MedicaSurvivinAntineoplastic AgentsApoptosisLigandsInhibitor of Apoptosis ProteinsBortezomibTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundSulindacExisulindNeoplasmsSurvivinmedicineAnimalsHumansbusiness.industryBortezomibapoptosis TRAIL/Apo2L apoptin/VP3 ONYX015 Bortezomib exisulind survivinCancerReceptors Death DomainHematologymedicine.diseaseBoronic AcidsNeoplasm ProteinsOncologyProteasomechemistryApoptosisPyrazinesCancer cellCancer researchCapsid ProteinsbusinessMicrotubule-Associated Proteinsmedicine.drug
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MYC and EGR1 synergize to trigger tumor cell death by controlling NOXA and BIM transcription upon treatment with the proteasome inhibitor bortezomib

2014

The c-MYC (MYC afterward) oncogene is well known for driving numerous oncogenic programs. However, MYC can also induce apoptosis and this function of MYC warrants further clarification. We report here that a clinically relevant proteasome inhibitor significantly increases MYC protein levels and that endogenous MYC is necessary for the induction of apoptosis. This kind of MYC-induced cell death is mediated by enhanced expression of the pro-apoptotic BCL2 family members NOXA and BIM. Quantitative promoter-scanning chromatin immunoprecipitations (qChIP) further revealed binding of MYC to the promoters of NOXA and BIM upon proteasome inhibition, correlating with increased transcription. Both pr…

Programmed cell deathTranscription GeneticEGR1ApoptosisBiologyBortezomibProto-Oncogene Proteins c-mycMicehemic and lymphatic diseasesCell Line TumorProto-Oncogene ProteinsGeneticsmedicineAnimalsPromoter Regions GeneticTranscription factorCells CulturedEarly Growth Response Protein 1Zinc finger transcription factorBinding SitesOncogeneBcl-2-Like Protein 11Genes p16Gene regulation Chromatin and EpigeneticsMembrane ProteinsPromoterGenes p53Boronic AcidsChromatinddc:Gene Expression Regulation NeoplasticProto-Oncogene Proteins c-bcl-2PyrazinesCancer researchProteasome inhibitorApoptosis Regulatory ProteinsProteasome Inhibitorsmedicine.drug
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7-Ketocholesterol Incorporation into Sphingolipid/Cholesterol-enriched (Lipid Raft) Domains Is Impaired by Vitamin E

2009

Cholesterol oxides, in particular 7-ketocholesterol, are proatherogenic compounds that induce cell death in the vascular wall when localized in lipid raft domains of the cell membrane. Deleterious effects of 7-ketocholesterol can be prevented by vitamin E, but the molecular mechanism involved is unclear. In this study, unlike γ-tocopherol, the α-tocopherol vitamin E form was found to prevent 7-ketocholesterol-mediated apoptosis of A7R5 smooth muscle cells. To be operative, α-tocopherol needed to be added to the cells before 7-ketocholesterol, and its anti-apoptotic effect was reduced and even suppressed when added together or after 7-ketocholesterol, respectively. Both pre- and co-treatment…

Programmed cell deathVitamin Emedicine.medical_treatmentfood and beveragesCell BiologyBiologyBiochemistrySphingolipidCell biologyCell membraneDephosphorylationchemistry.chemical_compoundmedicine.anatomical_structureBiochemistrychemistryApoptosismedicinelipids (amino acids peptides and proteins)alpha-TocopherolMolecular BiologyLipid raftJournal of Biological Chemistry
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Fatty acids liberated from low-density lipoprotein trigger endothelial apoptosis via mitogen-activated protein kinases.

2005

Enzymatic modification of low-density lipoprotein (LDL) as it probably occurs in the arterial intima drastically increases its cytotoxicity, which could be relevant for the progression of atherosclerotic lesions. LDL was treated with a protease and cholesterylesterase to generate a derivative similar to lesional LDL, with a high content of free cholesterol and fatty acids. Exposure of endothelial cells to the enzymatically modified lipoprotein (E-LDL), but not to native or oxidized LDL, resulted in programmed cell death. Apoptosis was triggered by apoptosis signal-regulating kinase 1 dependent phosphorylation of p38. Depletion and reconstitution experiments identified free fatty acids (FFA)…

Programmed cell deathp38 mitogen-activated protein kinasesBlotting WesternApoptosisDNA FragmentationBiologyFatty Acids NonesterifiedMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundHumansPhosphorylationMolecular BiologyCells CulturedCaspase 7Cell growthKinaseCaspase 3Cell BiologyCell biologyLipoproteins LDLchemistryBiochemistryApoptosisLow-density lipoproteinCaspasesPhosphorylationlipids (amino acids peptides and proteins)Endothelium VascularLipoproteinOleic AcidCell death and differentiation
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Role of oxoproline in the regulation of neutral amino acid transport across the blood-brain barrier.

1996

Regulation of neutral amino acid transport was studied using isolated plasma membrane vesicles derived from the bovine blood-brain barrier. Neutral amino acids cross the blood-brain barrier by facilitative transport system L1, which may allow both desirable and undesirable amino acids to enter the brain. The sodium-dependent amino acid systems A and Bo,+ are located exclusively on abluminal membranes, in a position to pump unwanted amino acids out. gamma-Glutamyl transpeptidase, the first enzyme of the gamma-glutamyl cycle, is an integral protein of the luminal membrane of the blood-brain barrier. We demonstrate that oxoproline, an intracellular product of the gamma-glutamyl cycle, stimulat…

ProlineBiologyBlood–brain barrierBiochemistrySystem aNeutral amino acid transportmedicineAnimalsAmino AcidsMolecular BiologyIntegral membrane proteinchemistry.chemical_classificationCell MembraneBiological TransportCell BiologyAmino acidCapillariesKineticsMembraneEnzymemedicine.anatomical_structureBiochemistrychemistryBlood-Brain BarrierCattleEndothelium VascularIntracellularThe Journal of biological chemistry
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Development of a second generation of inhibitors of microsomal prostaglandin E synthase 1 expression bearing the γ-hydroxybutenolide scaffold

2008

Petrosaspongiolide M (PM), a marine sesterterpene metabolite bearing the gamma-hydroxybutenolide scaffold and displaying a potent inhibitory activity toward PLA(2) enzyme, was selected by us as an attractive target in order to explore its mechanism of action at molecular level. In the course of our investigations we decided to synthetically modify the parent compound to clarify the structural determinants responsible for the activity; in fact, very recently, our research group reported the synthesis and the pharmacological properties of a first collection of PM analogues generated by Ludi approach. The synthesized compounds showed a poor or moderate activity toward PLA(2) enzymes, neverthel…

Prostaglandin AntagonistsStereochemistryMetaboliteClinical BiochemistryAnti-Inflammatory AgentsPharmaceutical ScienceIsomeraseProstaglandin E synthaseBiochemistryChemical synthesisCell LineMiceStructure-Activity Relationshipchemistry.chemical_compound4-ButyrolactoneMicrosomesDrug DiscoverymedicineAnimalsEnzyme InhibitorsProstaglandin E2Molecular BiologyProstaglandin-E Synthaseschemistry.chemical_classificationBinding SitesbiologyChemistryMacrophagesOrganic ChemistryIntramolecular OxidoreductasesPhospholipases A2EnzymeGene Expression RegulationMechanism of actionBiochemistryCyclooxygenase 2Enzyme inhibitorbiology.proteinMolecular Medicinelipids (amino acids peptides and proteins)medicine.symptommedicine.drugBioorganic & Medicinal Chemistry
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Enzymatically modified LDL induces cathepsin H in human monocytes: potential relevance in early atherogenesis.

2003

Objective—Modification with proteases and cholesterylesterase transforms LDL to a moiety that resembles lipoproteins isolated from atherosclerotic lesions and possesses atherogenic properties. To identify changes in monocyte-derived foam cells laden with enzymatically modified LDL (E-LDL), we compared patterns of the most abundant transcripts in these cells after incubation with LDL or E-LDL.Methods and Results—Serial analyses of gene expression (SAGE) libraries were constructed from human monocytes after treatment with LDL or E-LDL. Several tags were differentially expressed in LDL-treated versus E-LDL–treated cells, whereby marked selective induction by E-LDL of cathepsin H was conspicuou…

ProteasesCathepsin HCoronary Artery DiseaseBiologyCathepsin HCathepsin L1medicineMacrophageHumansFoam cellGene LibraryCathepsinMonocyteGene Expression ProfilingColocalizationSterol EsteraseMolecular biologyCathepsinsLipoproteins LDLCysteine Endopeptidasesmedicine.anatomical_structureCholesterolBiochemistryGene Expression Regulationlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineFoam CellsArteriosclerosis, thrombosis, and vascular biology
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