Search results for "hepatocyte"

showing 10 items of 369 documents

ER stress in human hepatic cells treated with Efavirenz: Mitochondria again

2013

Background & Aims ER stress is associated with a growing number of liver diseases, including drug-induced hepatotoxicity. The non-nucleoside analogue reverse transcriptase inhibitor Efavirenz, a cornerstone of the multidrug strategy employed to treat HIV1 infection, has been related to the development of various adverse events, including metabolic disturbances and hepatic toxicity, the mechanisms of which remain elusive. Recent evidence has pinpointed a specific mitochondrial effect of Efavirenz in human hepatic cells. This study assesses the induction of ER stress by Efavirenz in the same model and the implication of mitochondria in this process. Methods Primary human hepatocytes and Hep3B…

CyclopropanesEfavirenzXBP1Anti-HIV AgentsMitochondria LiverMitochondrionBiologyPharmacologyModels BiologicalCell Linechemistry.chemical_compoundMicroscopy Electron TransmissionDownregulation and upregulationHumansSide effectsEndoplasmic Reticulum Chaperone BiPCells CulturedHepatologyEndoplasmic reticulumHepatotoxicityATF4HIVEndoplasmic Reticulum StressHIV Reverse TranscriptaseBenzoxazinesMitochondriachemistryAlkynesHepatocytesHepatic stellate cellUnfolded protein responseReverse Transcriptase InhibitorsThapsigarginCalciumEfavirenzER stressBiomarkersJournal of Hepatology
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Inhibition of Mitochondrial Function by Efavirenz Increases Lipid Content in Hepatic Cells

2010

Efavirenz (EFV) is a non-nucleoside reverse transcriptase inhibitor (NNRTI) widely used in human immunodeficiency virus (HIV) infection therapy. It has been associated with hepatotoxic effects and alterations in lipid and body fat composition. Given the importance of the liver in lipid regulation, we have evaluated the effects of clinically used concentrations of EFV on the mitochondria and lipid metabolism of human hepatic cells in vitro. Mitochondrial function was rapidly undermined by EFV to an extent that varied with the concentration employed; in particular, respiration and intracellular adenosine triphosphate (ATP) levels were reduced whereas reactive oxygen species (ROS) production i…

CyclopropanesMaleEfavirenzAnti-HIV AgentsRespiratory chainMitochondria LiverPharmacologyBiologyMitochondrionNucleoside Reverse Transcriptase InhibitorRats Sprague-Dawleychemistry.chemical_compoundOxygen ConsumptionAMP-Activated Protein Kinase KinasesmedicineAnimalsHumansHepatologyAMPKLipid metabolismLipid MetabolismAdenosineLipidsBenzoxazinesRatschemistryBiochemistryAlkynesHepatocytesAdenosine triphosphateProtein Kinasesmedicine.drug
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Cellular cytotoxicity against autologous hepatocytes in alcoholic liver disease.

2008

We tested lymphocyte cytotoxicity against autologous hepatocytes in patients with alcoholic liver disease (ALD). The following cytotoxicity values were found (mean +/- SEM): alcohol-induced steatosis with or without fibrosis 16.5 +/- 2% (n = 29), alcoholic cirrhosis 28 +/- 4% (n = 13), controls with normal liver histology or minimal changes 6 +/- 2% (n = 11). The differences were statistically significant (both forms of ALD versus controls p less than 0.005). T-cell as well as non-T-cell-enriched lymphocyte fractions showed increased cytotoxicity in ALD. We did not observe a correlation between cellular cytotoxicity and the degree of biochemical or histological alterations within the groups…

Cytotoxicity ImmunologicAlcoholic liver diseasemedicine.medical_specialtyPathologyCirrhosisHepatologyLymphocyteHepatobiliary diseaseBiologyMiddle Agedmedicine.diseasemedicine.anatomical_structureEndocrinologyLiverFibrosisLiver Cirrhosis AlcoholicHepatocyteInternal medicinemedicineHumansSteatosisCytotoxicityFatty Liver AlcoholicT-Lymphocytes CytotoxicLiver
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Upregulation of Major Histocompatibility Complex Class I on Liver Cells by Hepatitis C Virus Core Protein via p53 and TAP1 Impairs Natural Killer Cel…

2003

ABSTRACTThe mechanisms of immune evasion and the role of the early immune response in chronic infection caused by hepatitis C virus (HCV) are still unclear. Here, we present evidence for a cascade of molecular events that the virus initiates to subvert the innate immune attack. The HCV core protein induced p53-dependent gene expression of TAP1 (transporter associated with antigen processing 1) and consecutive major histocompatibility complex (MHC) class I upregulation. Moreover, in p53-deficient liver cell lines, only reconstitution with wild-type p53, but not mutated p53 lacking DNA binding capacity, showed this effect. As a consequence of increased MHC class I expression, a significantly …

Cytotoxicity ImmunologicImmunologyAntigen presentationHepacivirusMajor histocompatibility complexMicrobiologyCell LineNatural killer cellAntigenVirologyMHC class ImedicineHumansATP Binding Cassette Transporter Subfamily B Member 2Cells CulturedLymphokine-activated killer cellbiologyViral Core ProteinsHistocompatibility Antigens Class IHepatitis C ChronicNatural killer T cellVirologyUp-RegulationKiller Cells Naturalmedicine.anatomical_structureInsect ScienceImmunologyHepatocytesbiology.proteinPathogenesis and ImmunityATP-Binding Cassette TransportersTumor Suppressor Protein p53CD8Journal of Virology
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Coordinated induction of drug transporters and phase I and II metabolism in human liver slices

2008

Although regulation of phase I drug metabolism in human liver is relatively well studied, the regulation of phase II enzymes and of drug transporters is incompletely characterized. Therefore, we used human liver slices to investigate the PXR, CAR and AhR-mediated induction of drug transporters and phase I and II metabolic enzymes. Precision-cut human liver slices were incubated for 5 or 24 h with prototypical inducers: phenobarbital (PB) (50 mu M) for CAR, beta-naphthoflavone (BNF) (25 mu M) for AhR, and rifampicin (RIF) (10 mu M) for PXR, and gene expression of the phase I enzymes CYP1A1, 1A2, 3A4, 3A5, 2136, 2A6, the phase II enzymes UGT1A1 and 1A6, and the transporters MRP2, MDR1, BSEP, …

DIFFERENTIAL REGULATIONQUANTITATIVE RT-PCRRAT-LIVERGene ExpressionPharmaceutical Sciencedrug transportersIn Vitro TechniquesPharmacologydigestive systemCytochrome P-450 Enzyme SystemUDP-GLUCURONOSYLTRANSFERASE 1A1Constitutive androstane receptorHumansSTELLATE CELL ACTIVATIONEnzyme inducerinductionliver slicesCONSTITUTIVE ANDROSTANE RECEPTORchemistry.chemical_classificationPregnane X receptorbiologyCYP3A4Multidrug resistance-associated protein 2TransporterPRIMARY HUMAN HEPATOCYTESMetabolic Detoxication Phase IIdrug metabolismEnzymeLiverPharmaceutical PreparationsBiochemistrychemistryEnzyme Inductionbiology.proteinMetabolic Detoxication Phase IPREGNANE-X-RECEPTORCarrier ProteinsPROTOTYPICAL INDUCERSDrug metabolismBILE-ACIDEuropean Journal of Pharmaceutical Sciences
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Replication of the hepatitis C virus

2000

Infection with the hepatitis C virus (HCV) is a major cause of chronic liver disease. HCV is an enveloped plus-strand RNA virus closely related to flavi- and pestiviruses. The first cloning of the HCV genome, about 10 years ago, initiated research efforts leading to the elucidation of the genomic organization and the definition of the functions of most viral proteins. Despite this progress the lack of convenient animal models and appropriate in vitro propagation systems have hampered a full understanding of the way the virus multiplies. This review summarizes our current knowledge about HCV replication and describes attempts pursued in the last few years to establish efficient and reliable …

DNA ReplicationbiologyHepatitis C virusGastroenterologyRNA virusGenome ViralHepacivirusHepatitis CVirus Replicationbiology.organism_classificationmedicine.diseasemedicine.disease_causeHepatitis CVirologyVirusFlaviviridaeViral replicationHepatocytesmedicineAnimalsHumansRNA ViralViral diseaseOncovirusBest Practice & Research Clinical Gastroenterology
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Thiocarbamate-Linked Polysulfonate–Peptide Conjugates As Selective Hepatocyte Growth Factor Receptor Binders

2014

The capacity of many proteins to interact with natural or synthetic polyanions has been exploited for modulating their biological action. However, the polydispersity of these macromolecular polyanions as well as their poor specificity is a severe limitation to their use as drugs. An emerging trend in this field is the synthesis of homogeneous and well-defined polyanion–peptide conjugates, which act as bivalent ligands, with the peptide part bringing the selectivity of the scaffold. Alternately, this strategy can be used for improving the binding of short peptides to polyanion-binding protein targets. This work describes the design and first synthesis of homogeneous polysulfonate–peptide con…

DendrimersBiomedical EngineeringPharmaceutical ScienceBioengineeringPeptidemacromolecular substancesPlasma protein bindingArticleReceptor tyrosine kinaseSubstrate SpecificityStructure-Activity RelationshipThiocarbamatesmedicineHumansStructure–activity relationshipPharmacologychemistry.chemical_classificationDose-Response Relationship DrugMolecular StructurebiologyHepatocyte Growth FactorChemistryOrganic Chemistrytechnology industry and agricultureProto-Oncogene Proteins c-metProtein Structure TertiaryThiocarbamateBiochemistryHepatocyte Growth Factor ReceptorProto-Oncogene Proteins c-metbiology.proteinHepatocyte growth factorSulfonic AcidsPeptidesProtein BindingBiotechnologymedicine.drugBioconjugate Chemistry
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Hepatic metabolism of diclofenac: role of human CYP in the minor oxidative pathways.

1999

The aim of this study was to re-examine the human hepatic metabolism of diclofenac, with special focus on the generation of minor hydroxylated metabolites implicated in the idiosyncratic hepatotoxicity of the drug. Different experimental approaches were used: human hepatocytes, human microsomes, and engineered cells expressing single human CYP (cytochromes P450). Human hepatocytes formed 3'-hydroxy-, 4'-hydroxy-, 5-hydroxy- 4',5-dihydroxy-, and N,5-dihydroxydiclofenac, as well as several lactams. Formation of 4'- and 5-hydroxydiclofenac by human liver microsomes followed a Michaelis-Menten kinetics (Km 9 +/- 1 microM; Vmax 432 +/- 15 pmol/min/mg and Km 43 +/- 5 microM; and Vmax 15.4 +/- 0.6…

DiclofenacMetaboliteIn Vitro TechniquesBiochemistryCell LineHydroxylationCytochrome P-450 CYP2C8chemistry.chemical_compoundTolbutamideCytochrome P-450 Enzyme SystemmedicineHumansBiotransformationCytochrome P-450 CYP2C9PharmacologybiologyAnti-Inflammatory Agents Non-SteroidalCytochrome P450Metabolismmedicine.anatomical_structureBiochemistrychemistrySteroid 16-alpha-HydroxylaseHepatocyteSteroid HydroxylasesMicrosomebiology.proteinMicrosomes LiverAryl Hydrocarbon HydroxylasesOxidation-ReductionDrug metabolismmedicine.drug
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Recombinant cDNA encapsulation in small liposomes with hepatocyte access ability.

1993

Liposomal encapsulation efficiency of a recombinant cDNA was studied by several procedures. We observed that supernatant fraction of ultracentrifuged liposomes prepared by extrusion through polycarbonate filters of 400 nm pore size yielded a very homogeneous suspension of small (50 nm diameter) unilamellar liposomes with highest DNA/lipid ratio and great ability to access to hepatocytes.

Drug CompoundingDNA RecombinantPharmaceutical ScienceBioengineeringBiologyIn Vitro Techniqueslaw.inventionchemistry.chemical_compoundMiceColloid and Surface ChemistrylawComplementary DNAmedicineAnimalsHumansPhysical and Theoretical ChemistryFluoresceinParticle SizeLiposomeDrug CarriersChromatographyParaffin EmbeddingStaining and LabelingOrganic ChemistryFluoresceinsMice Inbred C57BLMicroscopy Electronmedicine.anatomical_structureBiochemistrychemistryLiverHepatocytealpha 1-AntitrypsinLiposomesRecombinant DNAExtrusionParticle sizeDrug carrierFiltrationPlasmidsJournal of microencapsulation
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Hepatocytes--the choice to investigate drug metabolism and toxicity in man: in vitro variability as a reflection of in vivo.

2007

The pharmaceutical industry is committed to marketing safer drugs with fewer side effects, predictable pharmacokinetic properties and quantifiable drug-drug interactions. Drug metabolism is a major determinant of drug clearance and interindividual pharmacokinetic differences, and an indirect determinant of the clinical efficacy and toxicity of drugs. Progressive advances in the knowledge of metabolic routes and enzymes responsible for drug biotransformation have contributed to understanding the great metabolic variations existing in human beings. Phenotypic as well genotypic differences in the expression of the enzymes involved in drug metabolism are the main causes of this variability. How…

DrugDiclofenacDrug-Related Side Effects and Adverse Reactionsmedia_common.quotation_subjectBiologyPharmacologyIn Vitro TechniquesToxicologyModels BiologicalPharmacokineticsCytochrome P-450 Enzyme SystemIn vivoGenetic variationHumansDrug InteractionsPharmacokineticsBiotransformationCells Culturedmedia_commonMolecular StructureAnti-Inflammatory Agents Non-SteroidalCytochrome P450Genetic VariationGeneral MedicineIn vitroPharmaceutical PreparationsToxicityInactivation Metabolicbiology.proteinHepatocytesDrug metabolismMetabolic Networks and PathwaysChemico-biological interactions
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