Search results for " mito."

showing 10 items of 892 documents

Olive oils high in phenolic compounds modulate oxidative/antioxidative status in men

2004

The aim of the present study was to evaluate whether olive oils high in phenolic compounds influence the oxidative/antioxidative status in humans. Healthy men (n = 12) participated in a double-blind, randomized, crossover study in which 3 olive oils with low (LPC), moderate (MPC), and high (HPC) phenolic content were given as raw doses (25 mL/d) for 4 consecutive days preceded by 10-d washout periods. Volunteers followed a strict very low-antioxidant diet the 3 d before and during the intervention periods. Short-term consumption of olive oils decreased plasma oxidized LDL (oxLDL), 8-oxo-dG in mitochondrial DNA and urine, malondialdehyde in urine (P < 0.05 for linear trend), and increased HD…

AdultMaleTime FactorsMedicine (miscellaneous)Urinemedicine.disease_causeDNA MitochondrialAntioxidantschemistry.chemical_compoundDouble-Blind MethodPhenolsMalondialdehydemedicineHumansPlant OilsPhenolsFood scienceOlive OilGlutathione PeroxidaseNutrition and DieteticsCross-Over StudiesDose-Response Relationship DrugCholesterolCholesterol HDLDeoxyguanosineMalondialdehydePostprandial PeriodDietLipoproteins LDLDose–response relationshipVegetable oilPostprandialchemistryBiochemistry8-Hydroxy-2'-DeoxyguanosineOxidation-ReductionOxidative stress
researchProduct

Point mutations associated with Leber hereditary optic neuropathy in a Latvian population

2013

Purpose To study mutations associated with Leber hereditary optic neuropathy (LHON) in patients suspected of having this mitochondrial disorder in a Latvian population. Additional aims were to determine the heteroplasmy status of all non-synonymous polymorphisms identified in the current study and to identify the mitochondrial haplogroups of the studied participants because these factors may contribute to the manifestation of LHON. Methods Twelve patients, including patients in two families, were enrolled in the current study. LHON was suspected based on the findings of ophthalmologic examinations. In clinically affected individuals, the presence of all previously reported LHON-associated m…

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesPolymorphism Geneticgenetic structuresnutritional and metabolic diseasesOptic Atrophy Hereditary LeberSequence Analysis DNAMiddle AgedDNA MitochondrialLatviaeye diseasesWhite PeopleMitochondriaPedigreeHaplotypesHumansPoint MutationFemaleResearch Article
researchProduct

AZT treatment induces molecular and ultrastructural oxidative damage to muscle mitochondria. Prevention by antioxidant vitamins.

1998

AIDS patients who receive zidovudine (AZT) frequently suffer from myopathy. This has been attributed to mitochondrial (mt) damage, and specifically to the loss of mtDNA. This study examines whether AZT causes oxidative damage to DNA in patients and to skeletal muscle mitochondria in mice, and whether this damage may be prevented by supranutritional doses of antioxidant vitamins. Asymptomatic HIV-infected patients treated with AZT have a higher urinary excretion (355+/-100 pmol/kg/d) of 8-oxo-7, 8-dihydro-2'-deoxyguanosine (8-oxo-dG) (a marker of oxidative damage to DNA) than untreated controls (asymptomatic HIV-infected patients) (182+/-29 pmol/kg/d). This was prevented (110+/-79 pmol/kg/d)…

AdultMalemedicine.medical_specialtyDNA damageAnti-HIV Agentsmedicine.medical_treatmentAscorbic AcidBiologyDNA MitochondrialAntioxidantsZidovudinechemistry.chemical_compoundMiceInternal medicinemedicineDeoxyguanosineAnimalsHumansVitamin Eheterocyclic compoundsMyopathyVitamin ESkeletal musclevirus diseasesDeoxyguanosineGeneral MedicineGlutathioneHydrogen PeroxideAscorbic acidMitochondria Musclemedicine.anatomical_structureEndocrinologychemistryBiochemistry8-Hydroxy-2'-Deoxyguanosinemedicine.symptomZidovudinemedicine.drugDNA DamageResearch ArticleThe Journal of clinical investigation
researchProduct

Urinary 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxo-dG), a reliable oxidative stress marker in hypertension

2007

The potential use of oxidative stress products as disease markers and progression is an important aspect of biomedical research. In the present study, the quantification of urine 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dG) concentration has been used to express the oxidation status of hypertensive subjects. 8-oxo-dG has been simultaneously isolated and assayed in nuclear (nDNA) and mitochondrial DNA (mtDNA). In addition, oxidative stress of mononuclear cells has been estimated by means of GSH and GSSG levels and GSSG/GSH ratio in hypertensive subjects before and after antihypertensive treatment. It is shown that oxidative stress decreases significantly in hypertensive patients after trea…

AdultMalemedicine.medical_specialtyDNA damageUrinary systemUrinemedicine.disease_causeDNA MitochondrialBiochemistryPeripheral blood mononuclear cellchemistry.chemical_compoundInternal medicinemedicineHumansDeoxyguanosineChromatography High Pressure LiquidCell NucleusGlutathione DisulfideDeoxyguanosineGeneral MedicineGlutathioneGlutathioneOxidative StressEndocrinologychemistryBiochemistry8-Hydroxy-2'-DeoxyguanosineHypertensionGlutathione disulfideFemaleBiomarkersOxidative stressFree Radical Research
researchProduct

The UCP2 -866 G>A promoter region polymorphism is associated with nonalcoholic steatohepatitis

2015

Background & Aims Uncoupling protein 2 - UCP2 - regulates mitochondrial lipid fluxes and reactive oxygen species production by the respiratory chain. The −866 G>A UCP2 promoter region polymorphism has been linked to insulin resistance and lipid metabolism. The aim of this study was to assess whether the −866 G>A UCP2 polymorphism predisposes to nonalcoholic steatohepatitis in patients at risk, and the relationship with lipid metabolism and hepatic UCP2 expression. Methods We considered 688 Italian patients who underwent liver biopsy for suspected NASH, and 232 healthy controls. The UCP2 −866 G>A polymorphism was determined by allele specific oligonucleotide probes, hepatic UCP2 mRNA levels …

AdultMalemedicine.medical_specialtyGenotypeRespiratory chainGene ExpressionBiologyIon ChannelsMitochondrial Proteinsgenetic polymorphism; lipid metabolism;liver; mitochondria; nonalcoholic steatohepatitis; uncoupling protein-2Insulin resistanceNon-alcoholic Fatty Liver DiseaseRisk FactorsDiabetes mellitusInternal medicineGenotypemedicineHumansUncoupling Protein 2Promoter Regions GeneticUncoupling protein-2AllelesAgedPolymorphism GeneticGenetic polymorphismmedicine.diagnostic_testHepatologyLipid metabolismMiddle Agedmedicine.diseaseImpaired fasting glucoseMitochondriaEndocrinologyLogistic ModelsLipid metabolismLiverLiver biopsyCase-Control StudiesFemaleSteatosisInsulin ResistanceNonalcoholic steatohepatiti
researchProduct

Vitamin C and E supplementation alters protein signalling after a strength training session, but not muscle growth during 10 weeks of training

2014

This study investigated the effects of vitamin C and E supplementation on acute responses and adaptations to strength training. Thirty-two recreationally strength-trained men and women were randomly allocated to receive a vitamin C and E supplement (1000 mg day(-1) and 235 mg day(-1), respectively), or a placebo, for 10 weeks. During this period the participants' training involved heavy-load resistance exercise four times per week. Muscle biopsies from m. vastus lateralis were collected, and 1 repetition maximum (1RM) and maximal isometric voluntary contraction force, body composition (dual-energy X-ray absorptiometry), and muscle cross-sectional area (magnetic resonance imaging) were measu…

AdultMalemedicine.medical_specialtyJournal ClubPhysiologyStrength trainingMAP Kinase Signaling Systemmedicine.medical_treatmentMolecular and CellularMuscle ProteinsIsometric exerciseAscorbic AcidBiologyp38 Mitogen-Activated Protein KinasesMuscle hypertrophyIsometric ContractionInternal medicinemedicineHumansVitamin Eta315Leg pressMuscle SkeletalMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Vitamin Cta1184Vitamin EBiceps curlRibosomal Protein S6 Kinases 70-kDaResistance TrainingVitaminsAscorbic acidAdaptation PhysiologicalEndocrinologyDietary SupplementsFemale
researchProduct

Combination chemotherapy of 5-fluorouracil, epidoxorubicin and mitomycin C in the palliative treatment of locally advanced and/or metastatic adenocar…

1994

Thirty-seven consecutive patients with advanced and/or metastatic gastric adenocarcinoma received a combination of 5-fluorouracil 600 mg/m2 on days 1, 8, 29, 36; epidoxorubicin 75 mg/m2 i.v. on days 1, 29; mitomycin C 10 mg/m2 i.v. on day 1. This cycle was repeated every 8 weeks. Out of a total of 34 evaluable patients, 2 (5.8%) had a complete response and 7 (20.6%) had a partial response with an overall median duration of 40 weeks (range 20-128). The median survival of responding patients was not reached after a mean follow-up of 76 weeks, while that of patients with no change and progressive disease was reached at 36 and 13 weeks respectively. Treatment was generally well tolerated with h…

AdultMalemedicine.medical_specialtyMitomycinmedicine.medical_treatmentAdenocarcinomaGastric Adenocarcinoma Chemotherapy Epidoxorubicin Mitomicin CGastroenterologyStomach NeoplasmsInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansPharmacology (medical)Neoplasm MetastasisAgedEpirubicinAged 80 and overPharmacologyChemotherapybusiness.industryStomachPalliative CareMitomycin CCombination chemotherapyMiddle Agedmedicine.diseaseConfidence intervalSurgeryInfectious Diseasesmedicine.anatomical_structureOncologyFluorouracilAdenocarcinomaFemaleFluorouracilbusinessProgressive diseasemedicine.drug
researchProduct

Analysis of thiamine transporter genes in sporadic beriberi

2014

Abstract Objective Thiamine or vitamin B 1 deficiency diminishes thiamine-dependent enzymatic activity, alters mitochondrial function, impairs oxidative metabolism, and causes selective neuronal death. We analyzed for the first time, the role of all known mutations within three specific thiamine carrier genes, SLC19 A2, SLC19 A3 , and SLC25 A19 , in a patient with atrophic beriberi, a multiorgan nutritional disease caused by thiamine deficiency. Methods A 44-year-old male alcoholic patient from Morocco developed massive bilateral leg edema, a subacute sensorimotor neuropathy, and incontinence. Despite normal vitamin B 1 serum levels, his clinical picture was rapidly reverted by high-dose in…

AdultMalemedicine.medical_specialtySLC19 A- SLC25 A19SLC19 AEndocrinology Diabetes and MetabolismGene mutationBeriberimedicine.disease_causeMitochondrial Membrane Transport Proteinslaw.inventionBeriberilawInternal medicineGenotypemedicineThiamine transporterObjective: Thiamine or vitamin B1 deficiency diminishes thiamine-dependent enzymatic activity alters mitochondrial function impairs oxidative metabolism and causes selective neuronal death. We analyzed for the first time the role of all known mutations within three specific thiamine carrier genes SLC19 A2 SLC19 A3 and SLC25 A19 in a patient with atrophic beriberi a multiorgan nutritional disease caused by thiamine deficiency. Methods: A 44-year-old male alcoholic patient from Morocco developed massive bilateral leg edema a subacute sensorimotor neuropathy and incontinence. Despite normal vitamin B1 serum levels his clinical picture was rapidly reverted by high-dose intramuscular thiamine treatment suggesting a possible genetic resistance. We used polymerase chain reaction followed by amplicon sequencing to study all the known thiamine-related gene mutations identified within the Human Gene Mutation Database. Results: Thirty-seven mutations were tested: 29 in SLC19 A2 6 in SLC19 A3 and 2 in SLC25 A19. Mutational analyses showed a wild-type genotype for all sequences investigated. Conclusion: This is the first genetic study in beriberi disease. We did not detect any known mutation in any of the three genes in a sporadic dry beriberi patient. We cannot exclude a role for other known or unknown mutations in the same genes or in other thiamine-associated genes in the occurrence of this nutritional neuropathy.HumansThiamineGenePolymerase chain reactionGeneticsMutationNutrition and DieteticsbiologyMembrane Transport ProteinsThiamine Deficiencymedicine.diseaseAlcoholismEndocrinologyMutationbiology.proteinThiamineMutations
researchProduct

Maternally inherited diabetes and deafness (MIDD): unusual occult exocrine pancreatic manifestation in an affected German family

2000

The mitochondrial (mt) 3243 DNA mutation is an underlying cause of maternally inherited diabetes and deafness (MIDD) syndrome and the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). We report an affected German MIDD pedigree with maternal lineage over three generations. The index patient, her mother, her maternal aunt and her maternal grandmother all suffered from diabetes and premature hearing loss and were positive on testing for the mt 3243 DNA mutation. The 27-year-old index patient had a history of grand mal seizures. As sequela of abdominal ultrasound and confirmed by magnetic resonance cholangio-pancreaticography, she was diagnose…

AdultPathologymedicine.medical_specialtyPancreatic diseaseEndocrinology Diabetes and MetabolismEncephalopathyDeafnessMELAS syndromeDNA MitochondrialDiabetes ComplicationsEndocrinologyMitochondrial myopathyGermanyDiabetes MellitusInternal MedicineHumansMedicinePancreatic ductCommon bile ductbusiness.industryPancreatic DuctsCalcinosisPancreatic DiseasesSyndromeGeneral MedicineMiddle Agedmedicine.diseasePedigreemedicine.anatomical_structurePancreatitisLactic acidosisMutationPancreatitisFemalebusinessDilatation PathologicExperimental and Clinical Endocrinology &amp; Diabetes
researchProduct

Analysis of BNIP3 and BNIP3L/Nix expression in cybrid cell lines harboring two LHON-associated mutations.

2019

Mitochondria are key players in cell death through the activation of the intrinsic apoptosis pathway. BNIP3 and BNIP3L/Nix are outer mitochondrial membrane bifunctional proteins which because of containing both BH3 and LIR domains play a role in cellular response to stress by regulation of apoptosis and selective autophagy. Leber’s Hereditary Optic Neuropathy (LHON) is the most common mitochondrial disease in adults, characterized by painless loss of vision caused by atrophy of the optic nerve. The disease in over 90% of cases is caused by one of three mutations in the mitochondrial genome: 11778G&gt;A, 3460G&gt;A or 14484T&gt;C. The pathogenic processes leading to optic nerve degeneration …

AdultProgrammed cell deathMitochondrial diseaseApoptosisOptic Atrophy Hereditary LeberMitochondrionBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCell LineMitochondrial Proteins03 medical and health sciencesAtrophyProto-Oncogene ProteinsmedicineAutophagyHumans0303 health sciencesMutationTumor Suppressor Proteins030302 biochemistry & molecular biologyAutophagyIntrinsic apoptosisMembrane Proteinsmedicine.diseaseeye diseasesCell biologyApoptosisGenome MitochondrialMutationActa biochimica Polonica
researchProduct