Search results for "TOXICITY"

showing 10 items of 2261 documents

Profile of stress and toxicity gene expression in human hepatic cells treated with Efavirenz

2012

Hepatic toxicity and metabolic disorders are major adverse effects elicited during the pharmacological treatment of the human immunodeficiency virus (HIV) infection. Efavirenz (EFV), the most widely used non-nucleoside reverse transcriptase inhibitor (NNRTI), has been associated with these events, with recent studies implicating it in stress responses involving mitochondrial dysfunction and oxidative stress in human hepatic cells. To expand these findings, we analyzed the influence of EFV on the expression profile of selected stress and toxicity genes in these cells. Significant up-regulation was observed with Cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1), which indicated m…

CyclopropanesChemokineEfavirenzAnti-HIV AgentsPharmacologyMitochondrionmedicine.disease_causeCell Linechemistry.chemical_compoundStress PhysiologicalVirologyGene expressionmedicineHumansCXCL10PharmacologybiologyGene Expression ProfilingMolecular biologyBenzoxazinesMitochondriaOxidative StresschemistryAlkynesToxicityHepatocytesbiology.proteinHepatic stellate cellOxidative stressAntiviral Research
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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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Efavirenz induces interactions between leucocytes and endothelium through the activation of Mac-1 and gp150,95

2013

The potential cardiovascular (CV) toxicity associated with combined antiretroviral therapy (cART) has been attributed mainly to the nucleoside reverse transcriptase inhibitors abacavir and didanosine. However, the other two components of cART--non-nucleoside reverse transcriptase inhibitors (NNRTIs) and protease inhibitors (PIs)--may also be implicated, either directly or by influencing the action of the other drugs. This study evaluates the acute direct effects of the NNRTIs efavirenz and nevirapine and one of the most widely employed PIs, lopinavir, on leucocyte-endothelium interactions, a hallmark of CV disease.Drugs were analysed in vitro in human cells (interactions of peripheral blood…

CyclopropanesMaleMicrobiology (medical)EfavirenzNevirapineEndotheliumAnti-HIV AgentsIntegrin alphaXbeta2Macrophage-1 AntigenPharmacologyBiologyLopinavirNucleoside Reverse Transcriptase InhibitorRats Sprague-Dawleychemistry.chemical_compoundimmune system diseasesAbacavirCell AdhesionLeukocytesmedicineAnimalsHumansPharmacology (medical)EndotheliumNevirapineDidanosineCells CulturedPharmacologyGene Expression Profilingvirus diseasesLopinavirFlow CytometryBenzoxazinesRatsInfectious Diseasesmedicine.anatomical_structurechemistryAlkynesToxicitymedicine.drugJournal of Antimicrobial Chemotherapy
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Enhanced oxidative stress and increased mitochondrial mass during Efavirenz-induced apoptosis in human hepatic cells

2010

BACKGROUND AND PURPOSE Efavirenz (EFV) is widely used in the treatment of HIV-1 infection. Though highly efficient, there is growing concern about EFV-related side effects, the molecular basis of which remains elusive. EXPERIMENTAL APPROACH In vitro studies were performed to address the effect of clinically relevant concentrations of EFV (10, 25 and 50 mu M) on human hepatic cells. KEY RESULTS Cellular proliferation and viability were reduced in a concentration-dependent manner. Analyses of the cell cycle and several cell death parameters (chromatin condensation, phosphatidylserine exteriorization, mitochondrial proapoptotic protein translocation and caspase activation) revealed that EFV tr…

CyclopropanesMalehepatotoxicityCarcinoma HepatocellularTime FactorsAnti-HIV AgentsCell SurvivalApoptosisMitochondria LiverPhosphatidylserinesAntioxidantsSuperoxidesHumansChromansantiretroviral drugsCell Proliferationreactive oxygen speciesDose-Response Relationship DrugCell CycleLiver NeoplasmsChromatin Assembly and DisassemblyResearch PapersGlutathioneBenzoxazinesmitochondriaOxidative Stressside effectscell deathLiverAlkynesFemaleEfavirenzApoptosis Regulatory ProteinsHeLa Cells
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Involvement of nitric oxide in the mitochondrial action of efavirenz: a differential effect on neurons and glial cells

2014

Abstract The anti-human immunodeficiency virus (HIV) drug efavirenz (EFV) alters mitochondrial function in cultured neurons and glial cells. Nitric oxide (NO) is a mediator of mitochondrial dysfunction associated with HIV central nervous system symptoms. We show that EFV promotes inducible nitric oxide synthase (iNOS) expression in cultured glial cells and generated NO undermines their mitochondrial function, as inhibition of NOS partially reverses this effect. EFV inhibits mitochondrial Complex I in both neurons and glia; however, when the latter cells are treated for longer periods, other mitochondrial complexes are also affected in accordance with the increased NO production. These findi…

CyclopropanesNNRTIEfavirenzAnti-HIV AgentsCentral nervous systemNitric Oxide Synthase Type IIMitochondrionBiologyNitric OxideNitric oxideCell Linechemistry.chemical_compoundMediatornitric oxidemedicineImmunology and AllergyHumansNeuronsNeurotoxicityelectron transport chainHIVefavirenzmedicine.diseasecentral nervous systemCell biologyBenzoxazinesMitochondriaNitric oxide synthasemitochondriaInfectious Diseasesmedicine.anatomical_structurechemistryAlkynesImmunologybiology.proteinNeurogliaNeuroglia
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Applications of stable V79-derived cell lines expressing rat cytochromes P4501A1, 1A2, and 2B1.

1992

1. Chinese hamster V79-derived cell lines, stably expressing cytochromes P4501A1, 1A2, and 2B1 activities, were constructed by genetic engineering in continuation of our work to establish a battery of V79 derived cell lines designed to study the metabolism of xenobiotics. 2. Cell lines XEM1 and XEM2, expressing cytochrome P4501A1, were capable of the O-dealkylation of 7-ethoxycoumarin and the hydroxylation of benzo[a]pyrene. 3. Cell lines XEMd.MZ and XEMd.NH, expressing P4501A2, were shown to hydroxylate 17 beta-estradiol and 2-aminofluorene. 4. Cell line SD1, expressing cytochrome P4502B1, was able to hydroxylate testosterone stereo- and regio-specifically at the 16 alpha and 16 beta posit…

CytochromeHealth Toxicology and Mutagenesis78-Dihydro-78-dihydroxybenzo(a)pyrene 910-oxideGenetic VectorsDNA RecombinantHamsterHydroxylationToxicologyBiochemistryChinese hamsterlaw.inventionCell LineDihydroxydihydrobenzopyrenesMixed Function OxygenasesHydroxylationchemistry.chemical_compoundCricetulusCytochrome P-450 Enzyme SystemlawCytochrome P-450 CYP1A2CricetinaeBenzo(a)pyreneAnimalsCloning MolecularCytotoxicityCyclophosphamideBiotransformationPharmacologybiologyCytochrome P450General Medicinebiology.organism_classificationMolecular biologyRatsBiochemistrychemistryCell cultureRecombinant DNAbiology.proteinOxidoreductasesXenobiotica; the fate of foreign compounds in biological systems
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Bleomycin genotoxicity alteration by glutathione and cytochrome P-450 cellular content in respiratory proficient and deficient strains of Saccharomyc…

1999

The genotoxic effects of the antiblastic drug bleomycin were studied in the D7 strain of Saccharomyces cerevisiae and on its derivative mitochondrial mutant rho degree at different cellular concentrations of two drug metabolizing systems, glutathione (GSH) and cytochrome P-450. Bleomycin mutagenic activity was evaluated as frequencies of mitotic gene conversion, reversion and total aberrations under different physiological conditions. In the D7 strain, petite mutant induction was also detected. This is important due to the role of the mitochondrial genome in cancer induction, ageing and degenerative diseases. Both strains showed higher convertant than revertant induction. At high cytochrome…

CytochromeHealth Toxicology and MutagenesisSaccharomyces cerevisiaeMutantRespiratory chainCell Culture TechniquesSaccharomyces cerevisiaeToxicologymedicine.disease_causeBleomycinDNA Mitochondrialchemistry.chemical_compoundBleomycinOxygen ConsumptionCytochrome P-450 Enzyme SystemGeneticsmedicinePoint MutationGenetics (clinical)Chromosome AberrationsRecombination GeneticbiologyDose-Response Relationship DrugMutagenicity TestsCytochrome P450Glutathionebiology.organism_classificationGlutathioneBiochemistrychemistryMutagenesisbiology.proteinGenotoxicityMutagenesis
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T-CELL-MEDIATED CYTOLYSIS : FROM THE LYSIS OF H-2 NEGATIVE TARGET CELLS TO THE INDUCTIVE EFFECT OF XENOGENEIC SERUM

1979

Publisher Summary This chapter describes the results of a series of experiments. In the first series, evidence was found in favor of some specificity of cytolysis against embryonic antigens at the surface of the F9 cells. In a second series of experiments, it was found that P815 and EL4 cells were lysed. From a systematic investigation of the parameters of this system, two facts emerged. F9 cells were not necessary during the in vitro boost incubation. There was some preferential lysis of targets having the same H-2 as the mice receiving the H-2-less F9. For instance, if F9 cells were injected into B1O mice, and after 2–3 weeks, the spleen cells were incubated for 5 days in conventional tis…

CytolysisTissue culturemedicine.anatomical_structureLysisAntigenmedicineSpleenBiologyCytotoxicityEmbryonic stem cellMolecular biologyIn vitro
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Lymphocyte mediated cell lysis.

1989

Lymphocyte-mediated cell lysis represents an important immunologic effector mechanism involved in defense against viral infections, allograft rejection, and tumor surveillance. Moreover, regulatory T cell interactions within the immune system are based, at least in part, on molecular events related to this function. The multiplicity of effector cell populations that can mediate cytotoxicity, the cell/cell interaction determinants which they require for execution of their activities, and molecular events underlying the lytic process itself, as elucidated recently, are the subjects of the present review article.

Cytolytic granuleCytotoxicity ImmunologicEffectorRegulatory T cellLymphocyteCellGeneral MedicineBiologyCell biologymedicine.anatomical_structureImmune systemLytic cycleImmunologymedicineHumansLymphocytesCytotoxicityVirchows Archiv. B, Cell pathology including molecular pathology
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Nuclear Translocation of Mismatch Repair Proteins MSH2 and MSH6 as a Response of Cells to Alkylating Agents

2000

Mammalian mismatch repair has been implicated in mismatch correction, the prevention of mutagenesis and cancer, and the induction of genotoxicity and apoptosis. Here, we show that treatment of cells specifically with agents inducing O(6)-methylguanine in DNA, such as N-methyl-N'-nitro-N-nitrosoguanidine and N-methyl-N-nitrosourea, elevates the level of MSH2 and MSH6 and increases GT mismatch binding activity in the nucleus. This inducible response occurs immediately after alkylation, is long-lasting and dose-dependent, and results from translocation of the preformed MutSalpha complex (composed of MSH2 and MSH6) from the cytoplasm into the nucleus. It is not caused by an increase in MSH2 gen…

CytoplasmDNA RepairBase Pair MismatchRNA StabilityChromosomal translocationmedicine.disease_causeBiochemistrychemistry.chemical_compoundMismatch Repair Endonuclease PMS2Adenosine TriphosphatasesNuclear ProteinsMethylnitrosoureaNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinDNA mismatch repairMutL Protein Homolog 1Protein BindingAlkylating AgentsMethylnitronitrosoguanidinecongenital hereditary and neonatal diseases and abnormalitiesGuanineActive Transport Cell NucleusBiologyCell LineO(6)-Methylguanine-DNA MethyltransferaseProto-Oncogene ProteinsDNA Repair ProteinmedicineHumansRNA MessengerneoplasmsMolecular BiologyAdaptor Proteins Signal TransducingCell NucleusMutagenesisnutritional and metabolic diseasesDNACell BiologyDNA MethylationMolecular biologydigestive system diseasesMSH6DNA Repair EnzymesGene Expression RegulationchemistryMSH2Carrier ProteinsGenotoxicityDNADNA DamageHeLa CellsJournal of Biological Chemistry
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