Search results for "Mitochondrial disease"

showing 10 items of 34 documents

Mitochondria as the target for mildronate's protective effects in azidothymidine (AZT)-induced toxicity of isolated rat liver mitochondria

2008

Previously mildronate, an aza-butyrobetaine derivative, was shown to be a cytoprotective drug, through its mechanism of action of inhibition of carnitine palmitoyltransferase-1, thus protecting mitochondria from long-chain fatty acid accumulation and subsequent damage. Recently in an azidothymidine (AZT)-induced cardiotoxicity model in vivo (in mice), we have found mildronate's ability of protecting heart tissue from nuclear factor kappaB abnormal expression. Preliminary data also demonstrate cerebro- and hepatoprotecting properties of mildronate in AZT-toxicity models. We suggest that mildronate may target its action predominantly to mitochondria. The present study in isolated rat liver mi…

MaleMitochondrial DiseasesBioenergeticsAntimetabolitesCell RespirationClinical BiochemistryMitochondria LiverIn Vitro TechniquesMitochondrionPharmacologyBiologymedicine.disease_causeBiochemistryPermeabilityRespiratory electron transport chainDrug Delivery SystemsmedicineAnimalsCarnitineRats WistarCardiotoxicityCell BiologyGeneral MedicineRatsDisease Models AnimalMechanism of actionBiochemistryToxicitymedicine.symptomEnergy MetabolismZidovudineOxidative stressMethylhydrazinesmedicine.drug
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AZT induces oxidative damage to cardiac mitochondria: Protective effect of vitamins C and E

2004

Abstract AZT (zidovudine) is a potent inhibitor of HIV replication and a major antiretroviral drug used for AIDS treatment. A major limitation in the use of AZT is the occurrence of severe side effects. The aim of this work was to test whether AZT causes oxidative damage to heart mitochondria and whether this can be prevented by supranutritional doses of antioxidant vitamins. An experimental animal model was used in which mice were treated with AZT for 35 days (10 mg/kg/day) in drinking water. Animals treated with antioxidant vitamins were fed the same diet as controls but supplemented with vitamins C (ascorbic acid, 10 g/ kg diet) and E (α-dl-tocopherol, 0.6 g/kg diet) for 65 days before s…

MaleMitochondrial Diseasesmedicine.medical_treatmentAscorbic AcidOxidative phosphorylationMitochondrionPharmacologyBiologymedicine.disease_causeDNA MitochondrialMitochondria HeartGeneral Biochemistry Genetics and Molecular BiologyLipid peroxidationMiceZidovudinechemistry.chemical_compoundmedicineAnimalsVitamin Eheterocyclic compoundsGeneral Pharmacology Toxicology and PharmaceuticsVitamin CVitamin EDeoxyguanosineGeneral MedicineAscorbic acidGlutathioneBiochemistrychemistry8-Hydroxy-2'-DeoxyguanosineLipid PeroxidationZidovudineOxidative stressmedicine.drugLife Sciences
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A new mitochondrial point mutation in the transfer RNALys gene associated with progressive external ophthalmoplegia with impaired respiratory regulat…

2011

Abstract We report a novel heteroplasmic point mutation G8299A in the gene for mitochondrial tRNA Lys in a patient with progressive external ophthalmoplegia complicated by recurrent respiratory insufficiency. Biochemical analysis of respiratory chain complexes in muscle homogenate showed a combined complex I and IV deficiency. The transition does not represent a known neutral polymorphism and affects a position in the tRNA acceptor stem which is conserved in primates, leading to a destabilization of this functionally important domain. In vitro analysis of an essential maturation step of the tRNA transcript indicates the probable pathogenicity of this mutation. We hypothesize that there is a…

MaleOphthalmoplegia Chronic Progressive ExternalRNA MitochondrialMitochondrial diseaseMolecular Sequence DataRespiratory chainBiologymedicine.disease_causeSecondary PreventionmedicineHumansPoint MutationGeneticsMutationBase SequenceTransition (genetics)Point mutationExternal ophthalmoplegiaMiddle Agedmedicine.diseaseHeteroplasmyNeurologyRespiratory failureRNARNA Transfer LysNeurology (clinical)Respiratory InsufficiencyJournal of the Neurological Sciences
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Clinical manifestations and management of four children with Pearson syndrome.

2011

Pearson marrow-pancreas syndrome is a fatal disorder mostly diagnosed during infancy and caused by mutations of mitochondrial DNA. We hereby report on four children affected by Pearson syndrome with hematological disorders at onset. The disease was fatal to three of them and the fourth one, who received hematopoietic stem cell transplantation, died of secondary malignancy. In this latter patient transplantation corrected hematological and non-hematological issues like metabolic acidosis, and we therefore argue that it could be considered as a useful option in an early stage of the disease.

MalePediatricsmedicine.medical_specialtyMitochondrial DiseasesAnemiaMitochondrial diseasemedicine.medical_treatmenttrapianto cellule staminali emopoieticheHematopoietic stem cell transplantationDiseaseDNA MitochondrialLipid Metabolism Inborn Errorsmitochondrial disordersFatal OutcomeMuscular DiseasesCause of Deathhematopoietic stem cell transplantation; mitochondrial disorders; Pearson marrow-pancreas syndrome; trapianto cellule staminali emopoietiche; malattie mitocondriali; sindrome di PearsonGeneticsmedicineCongenital Bone Marrow Failure SyndromesHumansChildGenetics (clinical)Pearson marrow-pancreas syndromeCause of deathPearson syndromebusiness.industryAcyl-CoA Dehydrogenase Long-ChainHematopoietic Stem Cell TransplantationInfantMetabolic acidosissindrome di Pearsonmedicine.diseaseAnemia SideroblasticTransplantationChild PreschoolImmunologymalattie mitocondrialiFemalebusinessGene DeletionAmerican journal of medical genetics. Part A
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Autism and Intellectual Disability Associated with Mitochondrial Disease and Hyperlactacidemia

2015

Autism spectrum disorder (ASD) with intellectual disability (ID) is a life-long debilitating condition, which is characterized by cognitive function impairment and other neurological signs. Children with ASD-ID typically attain motor skills with a significant delay. A sub-group of ASD-IDs has been linked to hyperlactacidemia and alterations in mitochondrial respiratory chain activity. The objective of this report is to describe the clinical features of patients with these comorbidities in order to shed light on difficult diagnostic and therapeutic approaches in such patients. We reported the different clinical features of children with ID associated with hyperlactacidemia and deficiencies i…

Malemedicine.medical_specialtyPediatricsMitochondrial DiseasesUbiquinoneMitochondrial diseaseautismArticleCatalysislcsh:ChemistryInorganic Chemistrychemistry.chemical_compoundFolic AcidCarnitinemental disordersIntellectual disabilitymedicineHumansHyperlactatemiaCarnitinePhysical and Theoretical Chemistrypossible mitochondrial diseasePsychiatrylcsh:QH301-705.5Molecular BiologySpectroscopyCoenzyme Q10business.industryOrganic ChemistryInfantCognitionVitaminsGeneral Medicinemedicine.diseaseComputer Science ApplicationsMitochondrial respiratory chainlcsh:Biology (General)lcsh:QD1-999chemistryintellectual disabilityChild Development Disorders PervasiveAutism spectrum disorderChild Preschoolmuscular toneAutismFemalebusinessmedicine.drugInternational Journal of Molecular Sciences
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Mitochondrial interference by anti-HIV drugs: mechanisms beyond Pol-γ inhibition.

2011

The combined pharmacological approach to the treatment of HIV infection, known as highly active antiretroviral therapy (HAART), has dramatically reduced AIDS-related morbidity and mortality. However, its use has been associated with serious adverse reactions, of which those resulting from mitochondrial dysfunction are particularly widespread. Nucleos(t)ide-reverse transcriptase inhibitors (NRTIs) have long been considered the main source of HAART-related mitochondrial toxicity due to their ability to inhibit Pol-γ, the DNA polymerase responsible for the synthesis of mitochondrial DNA. Nevertheless, accumulating evidence points to a more complex relationship between these organelles and NRTI…

Mitochondrial DNAMitochondrial DiseasesNucleic Acid Synthesis InhibitorDNA polymeraseAnti-HIV Agentsmedicine.medical_treatmentDNA-Directed DNA PolymeraseMitochondrionPharmacologyToxicologyAntiretroviral Therapy Highly ActivemedicineAnimalsHumansNucleic Acid Synthesis InhibitorsPharmacologyProteasebiologyvirus diseasesmedicine.diseaseReverse transcriptaseDNA Polymerase gammaMitochondriaMitochondrial toxicityToxicitybiology.proteinReverse Transcriptase InhibitorsTrends in pharmacological sciences
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Ketogenic diet in neuromuscular and neurodegenerative diseases.

2014

An increasing number of data demonstrate the utility of ketogenic diets in a variety of metabolic diseases as obesity, metabolic syndrome, and diabetes. In regard to neurological disorders, ketogenic diet is recognized as an effective treatment for pharmacoresistant epilepsy but emerging data suggests that ketogenic diet could be also useful in amyotrophic lateral sclerosis, Alzheimer, Parkinson’s disease, and some mitochondriopathies. Although these diseases have different pathogenesis and features, there are some common mechanisms that could explain the effects of ketogenic diets. These mechanisms are to provide an efficient source of energy for the treatment of certain types of neurodege…

Mitochondrial Diseasesmedicine.medical_treatmentlcsh:MedicineDiseaseReview ArticleBiologyBioinformaticsGeneral Biochemistry Genetics and Molecular BiologyAlzheimer DiseaseDiabetes mellitusmedicineHumansAmyotrophic lateral sclerosisKetogenic diet metabolic diseases preventionGeneral Immunology and Microbiology3-Hydroxybutyric AcidAmyotrophic Lateral Sclerosislcsh:RBrainParkinson DiseaseGeneral Medicinemedicine.diseaseGlycogen Storage DiseaseObesityGlucoseMitochondrial biogenesisBiochemistryAlzheimer's diseaseMetabolic syndromeDiet KetogenicKetogenic diet
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Jaunu ģenētisko variantu funkcionāla raksturošana izmantojot izolētas pacientu šūnas

2022

Mutācijas gan mitohondriālajā DNS, gan kodola DNS var izraisīt traucējumus mitohondriju oksidatīvās fosforilēšanas sistēmā, kas var būt cēlonis smagām mitohondriālajām slimībām. Mitohondriālo slimību diagnostika ir komplicēta, un tai izmanto lielu laboratorijas metožu klāstu. Darba “JAUNU ĢENĒTISKO VARIANTU FUNKCIONĀLA RAKSTUROŠANA IZMANTOJOT IZOLĒTAS PACIENTU ŠŪNAS” mērķis ir raksturot jaunus ģenētiskos variantus reto ģenētisko slimību pacientiem, izmantojot molekulārās un bioķīmiskās metodes, kā arī perifēros leikocītus un kultivētus fibroblastus. Tika veikta DNS variantu validācija ar Sangera sekvencēšanu, šūnu līniju izveidošana un kultivēšana, mitohondriju izdalīšana no šūnu kultūrām u…

Mitohondriālās slimības/Mitochondrial diseasenDNS/nDNAģenētiskais variants/genetic variantBioloģijaOXPHOSmtDNS/mtDNA
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The role of glia, mitochondria, and the immune system in glaucoma.

2009

Author(s): Tezel, Gulgun; Fourth ARVO/Pfizer Ophthalmics Research Institute Conference Working Group

Nerve degenerationRetinal Ganglion Cellsmedicine.medical_specialtyMitochondrial Diseasesbusiness.industryGlaucomaGlaucomaMitochondrionmedicine.diseaseAxonsMitochondriaImmune systemOphthalmologyImmune SystemOptic Nerve DiseasesmedicineHumansbusinessOptic nerve diseasesNeurogliaInvestigative ophthalmologyvisual science
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Current Experience in Testing Mitochondrial Nutrients in Disorders Featuring Oxidative Stress and Mitochondrial Dysfunction: Rational Design of Chemo…

2014

An extensive number of pathologies are associated with mitochondrial dysfunction (MDF) and oxidative stress (OS). Thus, mitochondrial cofactors termed "mitochondrial nutrients" (MN), such as alpha-lipoic acid (ALA), Coenzyme Q10 (CoQ10), and L-carnitine (CARN) (or its derivatives) have been tested in a number of clinical trials, and this review is focused on the use of MN-based clinical trials. The papers reporting on MN-based clinical trials were retrieved in MedLine up to July 2014, and evaluated for the following endpoints: (a) treated diseases; (b) dosages, number of enrolled patients and duration of treatment; (c) trial success for each MN or MN combinations as reported by authors. The…

Pathologymedicine.medical_specialtyMitochondrial Diseasesmitochondrial nutrientsCoenzymesoxidative phosphorylationReviewPharmacologyMitochondrionBiologyControlled studiesmedicine.disease_causeChemopreventionCatalysislcsh:ChemistryInorganic Chemistrychemistry.chemical_compoundmitochondrial dysfunctionmedicineAnimalsHumansPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyCoenzyme Q10Clinical Trials as TopicOrganic ChemistryGeneral Medicine3. Good healthComputer Science ApplicationsMitochondriaClinical trialOxidative Stresslcsh:Biology (General)lcsh:QD1-999chemistrymitochondrial dysfunction and oxidative streKrebs cycleOxidative stressmitochondrial nutrient
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