Search results for "mitochondrial"

showing 10 items of 919 documents

Lon protease: a novel mitochondrial matrix protein in the interconnection between drug-induced mitochondrial dysfunction and endoplasmic reticulum st…

2017

Background and Purpose Mitochondria-associated membranes (MAMs) are specific endoplasmic reticulum (ER) domains that enable it to interact directly with mitochondria and mediate metabolic flow and Ca2+ transfer. A growing list of proteins have been identified as MAMs components, but how they are recruited and function during complex cell stress situations is still not understood, while the participation of mitochondrial matrix proteins is largely unrecognized. Experimental Approach This work compares mitochondrial/ER contact during combined ER stress/mitochondrial dysfunction using a model of human hepatoma cells (Hep3B cell line) treated for 24 h with classic pharmacological inducers of ER…

0301 basic medicinePharmacologyMitochondrial DNAChemistryEndoplasmic reticulumMitochondrionmedicine.diseaseCarbonyl cyanide m-chlorophenyl hydrazoneCell biology03 medical and health sciencesMitofusin-2chemistry.chemical_compound030104 developmental biology0302 clinical medicineMitochondrial matrixUnfolded protein responsemedicineOptic Atrophy 1030217 neurology & neurosurgeryBritish Journal of Pharmacology
researchProduct

Role of p62/SQSTM1 beyond autophagy: a lesson learned from drug-induced toxicity in vitro

2018

Background and Purpose SQSTM1/p62 is a multifunctional, stress-induced, scaffold protein involved in multiple cellular processes including autophagic clearance, regulation of inflammatory responses and redox homeostasis. Its altered function has been associated with different human pathologies, such as neurodegenerative, metabolic and bone diseases (down-regulation), and cancerogenesis (up-regulation). However, its role in the off-target effects of clinically used drugs is still not understood. Experimental Approach We evaluated the expression of p62 in cultured Hep3B cells and their derived ρ° cells (lacking mitochondria), along with markers of autophagy and mitochondrial dysfunction. The …

0301 basic medicinePharmacologyMitochondrial ROSScaffold proteinAutophagyATG5InflammasomePharmacologyMitochondrionBiologyCell biology03 medical and health sciences030104 developmental biologymedicineGene silencingViability assaymedicine.drugBritish Journal of Pharmacology
researchProduct

Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Compar…

2020

Reactive oxygen and nitrogen species (RONS) cause oxidative damage, which is associated with endothelial dysfunction and cardiovascular disease, but may also contribute to redox signaling. Therefore, their precise detection is important for the evaluation of disease mechanisms. Here, we compared three different methods for the detection of 3-nitrotyrosine (3-NT), a marker of nitro-oxidative stress, in biological samples. Nitrated proteins were generated by incubation with peroxynitrite or 3-morpholino sydnonimine (Sin-1) and subjected to total hydrolysis using pronase, a mixture of different proteases. The 3-NT was then separated by high performance liquid chromatography (HPLC) and quantifi…

0301 basic medicinePhysiologyClinical BiochemistryDot blotmitochondrial superoxidePronase030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryHigh-performance liquid chromatographyArticleperoxynitritePeroxynitrite03 medical and health sciences0302 clinical medicineProtein-bound 3-nitrotyrosinemedicineoxidative stressBovine serum albuminMolecular Biologychemistry.chemical_classificationDetection limitReactive oxygen speciesChromatographyHPLC with electrochemical detectionbiologylcsh:RM1-950Cell Biology3. Good health030104 developmental biologylcsh:Therapeutics. PharmacologychemistryOxidative stressbiology.proteinprotein-bound 3-nitrotyrosineOxidative stressEx vivoMitochondrial superoxide
researchProduct

Mitoprotective Clinical Strategies in Type 2 Diabetes and Fanconi Anemia Patients: Suggestions for Clinical Management of Mitochondrial Dysfunction

2020

Oxidative stress (OS) and mitochondrial dysfunction (MDF) occur in a number of disorders, and several clinical studies have attempted to counteract OS and MDF by providing adjuvant treatments against disease progression. The present review is aimed at focusing on two apparently distant diseases, namely type 2 diabetes (T2D) and a rare genetic disease, Fanconi anemia (FA). The pathogenetic links between T2D and FA include the high T2D prevalence among FA patients and the recognized evidence for OS and MDF in both disorders. This latter phenotypic/pathogenetic feature—namely MDF—may be regarded as a mechanistic ground both accounting for the clinical outcomes in both diseases, and…

0301 basic medicinePhysiologymedicine.medical_treatmentClinical Biochemistrymitochondrial nutrientsDiseaseType 2 diabetesReviewBioinformaticsmedicine.disease_causeBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineIn vivoFanconi anemiamitochondrial dysfunctionmedicineoxidative stressMolecular Biologyfanconi anemiaCoenzyme Q10business.industrylcsh:RM1-950Mitochondrial nutrientCell Biologymedicine.diseasePhenotype030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisOxidative stretype 2 diabetesbusinessAdjuvantOxidative stressAntioxidants
researchProduct

Effects of air pollution particles (ultrafine and fine particulate matter) on mitochondrial function and oxidative stress – Implications for cardiova…

2020

Environmental pollution is a major cause of global mortality and burden of disease. All chemical pollution forms together may be responsible for up to 12 million annual excess deaths as estimated by the Lancet Commission on pollution and health as well as the World Health Organization. Ambient air pollution by particulate matter (PM) and ozone was found to be associated with an all-cause mortality rate of up to 9 million in the year 2015, with the majority being of cerebro- and cardiovascular nature (e.g. stroke and ischemic heart disease). Recent evidence suggests that exposure to airborne particles and gases contributes to and accelerates neurodegenerative diseases. Especially, airborne t…

0301 basic medicinePollutionmedia_common.quotation_subjectBiophysicsAir pollutionEnvironmental pollutionDiseasemedicine.disease_causeBiochemistry03 medical and health sciencesEnvironmental healthMedicineAnimalsHumansEnvironmental risk factorsNeurodegenerationMolecular Biologymedia_commonMitochondrial damage and dysfunctionAir Pollutants030102 biochemistry & molecular biologybusiness.industryMortality rateNeurodegenerationNeurodegenerative DiseasesParticulatesmedicine.diseaseCardiovascular diseaseMitochondriaOxidative Stress030104 developmental biologyCardiovascular DiseasesAmbient air pollution; Cardiovascular disease; Environmental risk factors; Mitochondrial damage and dysfunction; Neurodegeneration; Particulate matter; Air Pollutants; Animals; Cardiovascular Diseases; Humans; Mitochondria; Neurodegenerative Diseases; Oxidative Stress; Particulate MatterParticulate MatterAmbient air pollutionbusinessOxidative stress
researchProduct

Enzymatic Spermine Metabolites Induce Apoptosis Associated with Increase of p53, caspase-3 and miR-34a in Both Neuroblastoma Cells, SJNKP and the N-M…

2021

Neuroblastoma (NB) is a common malignant solid tumor in children and accounts for 15% of childhood cancer mortality. Amplification of the N-Myc oncogene is a well-established poor prognostic marker in NB patients and strongly correlates with higher tumor aggression and resistance to treatment. New therapies for patients with N-Myc-amplified NB need to be developed. After treating NB cells with BSAO/SPM, the detection of apoptosis was determined after annexin V-FITC labeling and DNA staining with propidium iodide. The mitochondrial membrane potential activity was checked, labeling cells with the probe JC-1 dye. We analyzed, by real-time RT-PCR, the transcript of genes involved in the apoptot…

0301 basic medicinePolyamine; neuroblastoma; apoptosis; microRNA; mitochondria; reactive oxygen species; oncotherapychemistry.chemical_compound0302 clinical medicineAnnexinpolyamineSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaBiology (General)Membrane Potential Mitochondrialreactive oxygen speciesN-Myc Proto-Oncogene ProteinmicroRNAChemistryCaspase 3apoptosisGeneral MedicineBlotGene Expression Regulation Neoplasticmitochondria030220 oncology & carcinogenesisAmine Oxidase (Copper-Containing)Signal TransductiononcotherapyQH301-705.5Caspase 3apoptosis; microRNA; mitochondria; neuroblastoma; oncotherapy; polyamine; reactive oxygen species.ArticleNO03 medical and health sciencesneuroblastomaNeuroblastomaCell Line TumormedicineAnimalsHumansPropidium iodideRats WistarCell ProliferationOncogeneGene Amplificationmedicine.diseaseapoptosis; microRNA; mitochondria; neuroblastoma; oncotherapy; polyamine; reactive oxygen speciesMolecular biologyMicroRNAs030104 developmental biologyApoptosisSpermineTumor Suppressor Protein p53
researchProduct

Mitochondrial DNA Replacement Techniques to Prevent Human Mitochondrial Diseases.

2021

Background: Mitochondrial DNA (mtDNA) diseases are a group of maternally inherited genetic disorders caused by a lack of energy production. Currently, mtDNA diseases have a poor prognosis and no known cure. The chance to have unaffected offspring with a genetic link is important for the affected families, and mitochondrial replacement techniques (MRTs) allow them to do so. MRTs consist of transferring the nuclear DNA from an oocyte with pathogenic mtDNA to an enucleated donor oocyte without pathogenic mtDNA. This paper aims to determine the efficacy, associated risks, and main ethical and legal issues related to MRTs. Methods: A bibliographic review was performed on the MEDLINE and Web of S…

0301 basic medicinePoor prognosisLegal positionMitochondrial DNAFarmacologiaWeb of scienceMEDLINEReviewmitochondrial DNABioinformaticsDNA MitochondrialCatalysisMitocondrisInorganic Chemistrylcsh:Chemistry03 medical and health sciencesmitochondrial donation0302 clinical medicineMedicineHumansPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5Spectroscopymitochondrial diseases030219 obstetrics & reproductive medicinebusiness.industryOrganic ChemistryDonor oocyteGeneral MedicineDNAGenetic TherapyComputer Science ApplicationsNuclear DNAMitochondriaClinical trial030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Oocytesmitochondrial replacementthree-parent babybusinessInternational journal of molecular sciences
researchProduct

Dynamic evolution of mitochondrial genomes in Trebouxiophyceae, including the first completely assembled mtDNA from a lichen-symbiont microalga (Treb…

2019

AbstractTrebouxiophyceae (Chlorophyta) is a species-rich class of green algae with a remarkable morphological and ecological diversity. Currently, there are a few completely sequenced mitochondrial genomes (mtDNA) from diverse Trebouxiophyceae but none from lichen symbionts. Here, we report the mitochondrial genome sequence of Trebouxia sp. TR9 as the first complete mtDNA sequence available for a lichen-symbiont microalga. A comparative study of the mitochondrial genome of Trebouxia sp. TR9 with other chlorophytes showed important organizational changes, even between closely related taxa. The most remarkable change is the enlargement of the genome in certain Trebouxiophyceae, which is princ…

0301 basic medicinePrasiolalesTrebouxiaMitochondrial DNALichensEvolutionlcsh:MedicineBiologyDNA MitochondrialGenomeArticleEvolution MolecularOpen Reading Frames03 medical and health sciences0302 clinical medicineIntergenic regionSpecies SpecificityChlorophytaPhylogeneticsMicroalgaelcsh:SciencePhylogenyMultidisciplinaryTrebouxiophyceaelcsh:RSequence Analysis DNAGroup II intronbiology.organism_classificationIntrons030104 developmental biologyTandem Repeat SequencesEvolutionary biologyGenome Mitochondriallcsh:QPlant sciences030217 neurology & neurosurgeryScientific Reports
researchProduct

Attenuation of 7-ketocholesterol- and 7β-hydroxycholesterol-induced oxiapoptophagy by nutrients, synthetic molecules and oils: Potential for the prev…

2021

Age-related diseases for which there are no effective treatments include cardiovascular diseases; neurodegenerative diseases such as Alzheimer's disease; eye disorders such as cataract and age-related macular degeneration; and, more recently, Severe Acute Respiratory Syndrome (SARS-CoV-2). These diseases are associated with plasma and/or tissue increases in cholesterol derivatives mainly formed by auto-oxidation: 7-ketocholesterol, also known as 7-oxo-cholesterol, and 7β-hydroxycholesterol. The formation of these oxysterols can be considered as a consequence of mitochondrial and peroxisomal dysfunction, leading to increased in oxidative stress, which is accentuated with age. 7-ketocholester…

0301 basic medicineProgrammed cell deathAgingOxysterolMitochondrionPharmacologymedicine.disease_causeBiochemistry03 medical and health sciences0302 clinical medicineLysosomemedicineHumansMolecular BiologyKetocholesterolsChemistrySARS-CoV-2COVID-19NutrientsPeroxisomeHydroxycholesterols030104 developmental biologymedicine.anatomical_structureNeurologyMitochondrial permeability transition poreEye disorderlipids (amino acids peptides and proteins)Oils030217 neurology & neurosurgeryOxidative stressBiotechnologyAgeing research reviews
researchProduct

Transcriptomic study of the toxic mechanism triggered by beauvericin in Jurkat cells

2018

Beauvericin (BEA), an ionophoric cyclic hexadepsipeptide mycotoxin, is able to increase oxidative stress by altering membrane ion permeability and uncoupling oxidative phosphorylation. A toxicogenomic study was performed to investigate gene expression changes triggered by BEA exposure (1.5, 3 and 5 mu M; 24 h) in Jurkat cells through RNA-sequencing and differential gene expression analysis. Perturbed gene expression was observed in a concentration dependent manner, with 43 differentially expressed genes (DEGs) overlapped in the three studied concentrations. Gene ontology (GO) analysis showed several biological processes related to electron transport chain, oxidative phosphorylation, and cel…

0301 basic medicineProgrammed cell deathCYTOCHROME-C RELEASEBCL-2 FAMILYCell Membrane PermeabilityRespiratory chainCell Culture TechniquesCASPASE-3 ACTIVATIONApoptosisOxidative phosphorylationCHO-K1 CELLSToxicologyJurkat cellsOxidative PhosphorylationElectron Transport03 medical and health sciencesJurkat CellsFUSARIUM MYCOTOXINSImmunotoxicologyDepsipeptidesHumansREAL-TIME PCROXIDATIVE STRESSTranscriptomicsCaspaseINDUCED APOPTOSISLEUKEMIA-CELLS030102 biochemistry & molecular biologybiologyDose-Response Relationship DrugChemistryJurkatGene Expression ProfilingBcl-2 familyDEATHGeneral MedicineBeauvericinToxicogenomicsCell biologyGene expression profiling030104 developmental biologyMitochondrial respiratory chainGene Ontologybiology.proteinRNA-seqTranscriptomeToxicology Letters
researchProduct