Search results for "neurotoxicity"

showing 10 items of 105 documents

Adaptogens in chemobrain (Part I): Plant extracts attenuate cancer chemotherapy-induced cognitive impairment – Transcriptome-wide microarray profiles…

2019

Abstract Background Cancer chemotherapy-induced cognitive impairments are presumably associated with undesirable effects of chemotherapy on physiological functions of brain cells. Adaptogens are natural compounds or plant extracts increasing an organism's adaptability and survival in stress. They exhibited neuroprotective effects and increased cognitive functions in clinical studies in human beings. Hypothesis We hypothesized that selected adaptogenic plant extracts attenuate or prevent cancer chemotherapy-induced cognitive impairments. Aim We assessed the effects of selected adaptogenic herbal extracts on FEC (fixed combination 5-fluorouracil, epirubicin and cyclophosphamide) induced chang…

MicroarrayPharmaceutical ScienceBiologyPharmacologyNeuroprotectionCell LineTranscriptome03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsDrug DiscoverymedicineHumansCognitive DysfunctionCyclophosphamideEpirubicinOligonucleotide Array Sequence AnalysisSchisandra030304 developmental biologyPharmacology0303 health sciencesPlant ExtractsMicroarray analysis techniquesGene Expression ProfilingAxon extensionNeurogenesisGene expression profilingmedicine.anatomical_structureGene Expression RegulationComplementary and alternative medicineFruit030220 oncology & carcinogenesisMolecular MedicineNeurogliaAndrographisNeurotoxicity SyndromesRhodiolaFluorouracilDiterpenesNeurogliaPhytomedicine
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The role of mycotoxins in neurodegenerative diseases: current state of the art and future perspectives of research

2021

Abstract Mycotoxins are fungal metabolites that can cause various diseases in humans and animals. The adverse health effects of mycotoxins such as liver failure, immune deficiency, and cancer are well-described. However, growing evidence suggests an additional link between these fungal metabolites and neurodegenerative diseases. Despite the wealth of these initial reports, reliable conclusions are still constrained by limited access to human patients and availability of suitable cell or animal model systems. This review summarizes knowledge on mycotoxins associated with neurodegenerative diseases and the assumed underlying pathophysiological mechanisms. The limitations of the common in vivo…

business.industryClinical BiochemistryFungiLiver failureNeurotoxicityfood and beveragesNeurodegenerative DiseasesMycotoxinsBioinformaticsmedicine.diseaseBiochemistryLimited accesschemistry.chemical_compoundAnimal modelchemistryAdverse health effectAnimalsHumansMedicinebusinessMycotoxinMolecular BiologyBiological Chemistry
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Toxicity of mycotoxins in vivo on vertebrate organisms: A review.

2019

Mycotoxins are considered to be a major risk factor affecting human and animal health as they are one of the most dangerous contaminants of food and feed. This review aims to compile the research developed up to date on the toxicological effects that mycotoxins can induce on human health, through the examination of a selected number of studies in vivo. AFB1 shows to be currently the most studied mycotoxin in vivo, followed by DON, ZEA and OTA. Scarce data was found for FBs, PAT, CIT, AOH and Fusarium emerging mycotoxins. The majority of them concerned the investigation of immunotoxicity, whereas the rest consisted in the study of genotoxicity, oxidative stress, hepatotoxicity, cytotoxicity,…

FusariumMicroarrayPharmacologyToxicologymedicine.disease_causeChemistry Techniques AnalyticalTranscriptome03 medical and health scienceschemistry.chemical_compound0404 agricultural biotechnologyIn vivomedicineAnimalsHumansMycotoxin030304 developmental biology0303 health sciencesbiologyNeurotoxicityfood and beverages04 agricultural and veterinary sciencesGeneral MedicineMycotoxinsbiology.organism_classificationmedicine.disease040401 food sciencechemistryToxicityGenotoxicityFood ScienceFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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Neurotoxicity of zearalenone’s metabolites and beauvericin mycotoxins via apoptosis and cell cycle disruption

2021

Cell cycle progression and programmed cell death are imposed by pathological stimuli of extrinsic or intrinsic including the exposure to neurotoxins, oxidative stress and DNA damage. All can cause abrupt or delayed cell death, inactivate normal cell survival or cell death networks. Nevertheless, the mechanisms of the neuronal cell death are unresolved. One of the cell deaths triggers which have been wildly studied, correspond to mycotoxins produced by Fusarium species, which have been demonstrated cytotoxicity and neurotoxicity through impairing cell proliferation, gene expression and induction of oxidative stress. The aim of present study was to analyze the cell cycle progression and cell …

0301 basic medicineProgrammed cell deathCellPopulationApoptosisToxicology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorDepsipeptidesmedicineHumansEstrogens Non-SteroidaleducationCell Proliferationeducation.field_of_studyCell growthCell CycleNeurotoxicityMycotoxinsCell cyclemedicine.diseaseMolecular biologyBeauvericin030104 developmental biologymedicine.anatomical_structurechemistryApoptosisZearalenone030217 neurology & neurosurgeryToxicology
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Prevention of 7-Ketocholesterol-Induced Overproduction of Reactive Oxygen Species, Mitochondrial Dysfunction and Cell Death with Major Nutrients (Pol…

2020

The brain, which is a cholesterol-rich organ, can be subject to oxidative stress in a variety of pathophysiological conditions, age-related diseases and some rare pathologies. This can lead to the formation of 7-ketocholesterol (7KC), a toxic derivative of cholesterol mainly produced by auto-oxidation. So, preventing the neuronal toxicity of 7KC is an important issue to avoid brain damage. As there are numerous data in favor of the prevention of neurodegeneration by the Mediterranean diet, this study aimed to evaluate the potential of a series of polyphenols (resveratrol, RSV

eicosapentaenoic acidPharmaceutical ScienceResveratrolDiet Mediterraneanmedicine.disease_causequercetinAnalytical ChemistryMicechemistry.chemical_compound0302 clinical medicineDrug Discoveryoxidative stressKetocholesterolsNeuronschemistry.chemical_classification0303 health sciencesCell Deathfood and beveragesdocosahexaenoic acidEicosapentaenoic acidMitochondriaBiochemistryChemistry (miscellaneous)Docosahexaenoic acid030220 oncology & carcinogenesisMolecular Medicineα-linolenic acidN2a cellsArticlelcsh:QD241-44103 medical and health sciencesresveratrol.lcsh:Organic chemistryCell Line TumorMediterranean dietFatty Acids Omega-3medicineAnimalsPropidium iodidePhysical and Theoretical Chemistry7-ketocholesterol030304 developmental biologyapigeninReactive oxygen speciesOrganic ChemistryNeurotoxicityPolyphenolsmedicine.diseaseOleic acidoleic acidchemistryReactive Oxygen SpeciesOxidative stressMolecules
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Interaction between 24-hydroxycholesterol, oxidative stress, and amyloid-β in amplifying neuronal damage in Alzheimer’s disease: three partners in cr…

2011

All three cholesterol oxidation products implicated thus far in the pathogenesis of Alzheimer's disease, 7β-hydroxycholesterol, 24-hydroxycholesterol, and 27-hydroxycholesterol, markedly enhance the binding of amyloid-beta (Aβ) to human differentiated neuronal cell lines (SK-N-BE and NT-2) by up-regulating net expression and synthesis of CD36 and β1-integrin receptors. However, only 24-hydroxycholesterol markedly potentiates the pro-apoptotic and pro-necrogenic effects of Aβ(1-42) peptide on these cells: 7β-hydroxycholesterol and 27-hydroxycholesterol, like unoxidized cholesterol, show no potentiating effect. This peculiar behavior of 24-hydroxycholesterol at physiologic concentrations (1 μ…

chemistry.chemical_classificationAgingReactive oxygen speciesbiologyCD36NeurotoxicityLong-term potentiationCell BiologyGlutathionemedicine.diseasemedicine.disease_causeCell biologychemistry.chemical_compoundchemistryBiochemistrypolycyclic compoundsbiology.proteinmedicinelipids (amino acids peptides and proteins)ReceptorOxidative stressIntracellularAging Cell
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In vivo and in vitro effects of multiple sclerosis immunomodulatory therapeutics on glutamatergic excitotoxicity.

2015

In multiple sclerosis (MS), a candidate downstream mechanism for neuronal injury is glutamate (Glu)-induced excitotoxicity, leading to toxic increases in intraneuronal Ca(2+) . Here, we used in vivo two-photon imaging in the brain of TN-XXL transgenic Ca(2+) reporter mice to test whether promising oral MS therapeutics, namely fingolimod, dimethyl fumarate, and their respective metabolites fingolimod-phosphate and monomethyl fumarate, can protect neurons against acute glutamatergic excitotoxic damage. We also assessed whether these drugs can protect against excitotoxicity in vitro using primary cortical neurons, and whether they can directly inhibit Glu release from pathogenic T-helper 17 ly…

0301 basic medicineKainic acidMultiple SclerosisExcitotoxicityGlutamic AcidPharmacologyBiologymedicine.disease_causeBiochemistryNeuroprotectionImmunomodulation03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineIn vivomedicineAnimalsCells CulturedNeuronsKainic AcidDimethyl fumarateCell DeathGlutamate receptorNeurotoxicityBrainmedicine.diseaseUp-Regulation030104 developmental biologyNeuroprotective AgentschemistryNMDA receptor030217 neurology & neurosurgerySignal TransductionJournal of neurochemistry
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Oxidative Stress, a Crossroad Between Rare Diseases and Neurodegeneration

2020

Oxidative stress is an imbalance between production and accumulation of oxygen reactive species and/or reactive nitrogen species in cells and tissues, and the capacity of detoxifying these products, using enzymatic and non-enzymatic components, such as glutathione. Oxidative stress plays roles in several pathological processes in the nervous system, such as neurotoxicity, neuroinflammation, ischemic stroke, and neurodegeneration. The concepts of oxidative stress and rare diseases were formulated in the eighties, and since then, the link between them has not stopped growing. The present review aims to expand knowledge in the pathological processes associated with oxidative stress underlying …

0301 basic medicineAtaxiaUnverricht–Lundborg disease (ULD)PhysiologyNeurodegeneration with brain iron accumulationClinical BiochemistryFriedreich’s ataxiaReviewmedicine.disease_causeBioinformaticsBiochemistry03 medical and health scienceschemistry.chemical_compoundLafora disease (LD)0302 clinical medicineMedicineprogressive myoclonus epilepsy (PME)Molecular BiologyNeuroinflammationReactive nitrogen speciesneurodegenerative disorders with brain iron accumulation (NBIA)business.industryNeurodegenerationlcsh:RM1-950NeurotoxicityCell Biologymedicine.diseaseDravet syndromeCharcot-Marie-Tooth disease (CMT)030104 developmental biologylcsh:Therapeutics. Pharmacologychemistrymedicine.symptombusinessMyoclonusinherited retinal dystrophy (IRD)030217 neurology & neurosurgeryOxidative stressAntioxidants
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Designing trehalose-conjugated peptides for the inhibition of Alzheimer’s Aβ oligomerization and neurotoxicity

2008

Neurotoxicity Alzheimer Amyloidsbeta-sheet breaker peptides • amyloid-beta • trehalose • SFM • neuronal cultures • thioflavin T
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Inactivation of glycogen synthase kinase-3β protects against kainic acid-induced neurotoxicity in vivo

2004

Many neurodegenerative diseases involve oxidative stress and excitotoxic cell death. In an attempt to further elucidate the signal transduction pathways involved in the cell death/cell survival associated with excitotoxicity, we have used an in vivo model of excitotoxicity employing kainic acid (KA)-induced neurotoxicity. Here, we show that extracellular signal-related kinase (ERK) 2, but not ERK 1, is phosphorylated and thereby activated in the hippocampus and cerebellum of kainic acid-treated mice. Phosphorylation and hence inactivation of glycogen synthase kinase 3beta (GSK-3beta), a general survival factor, is often a downstream consequence of mitogen-activated protein kinase pathway ac…

MaleMAPK/ERK pathwayKainic acidProgrammed cell deathTime FactorsCell SurvivalBlotting WesternExcitotoxicityTetrazolium Saltsmacromolecular substancesBiologymedicine.disease_causeHippocampusGlycogen Synthase Kinase 3Micechemistry.chemical_compoundOrgan Culture TechniquesGSK-3CerebellumNitrilesButadienesSerinemedicineAnimalsEnzyme InhibitorsPhosphorylationProtein kinase AMolecular BiologyMitogen-Activated Protein Kinase 1Glycogen Synthase Kinase 3 betaKainic AcidBehavior AnimalCell DeathKinaseGeneral NeuroscienceImmunohistochemistryCell biologyEnzyme ActivationThiazolesBiochemistrychemistryTyrosineNeurotoxicity SyndromesNeurology (clinical)Signal transductionLithium ChlorideDevelopmental BiologyBrain Research
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