0000000000759567

AUTHOR

Michael Ristow

0000-0003-2109-2453

showing 3 related works from this author

Antioxidant supplements in exercise: worse than useless?

2012

TO THE EDITOR: In a recent paper by Higashida et al. (5), the authors report that very large doses of antioxidant vitamins do not prevent the exercise-induced adaptive responses of muscle mitochondria, GLUT4, and insulin action to exercise. As clearly stated in the paper, their data disagree with those reported by three independent research groups from Germany (14), Australia (17), and Spain (4). Using a significantly different experimental protocol regarding exercise training intensity and duration, antioxidant supplementation (doses and types of antioxidants), and molecular parameters analyzed (mRNA vs. protein levels), Higashida et al. compared their data with ours and came to exactly th…

medicine.medical_specialtyAntioxidantVitamin CbiologyPhysiologybusiness.industryEndocrinology Diabetes and Metabolismmedicine.medical_treatmentInsulinSkeletal muscleClinical nutritionmedicine.anatomical_structureEndocrinologyMitochondrial biogenesisPhysiology (medical)Internal medicinemedicinebiology.proteinbusinessInhibitory effectGLUT4American Journal of Physiology-Endocrinology and Metabolism
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40(th) EASD Annual Meeting of the European Association for the Study of Diabetes : Munich, Germany, 5-9 September 2004

2004

0303 health sciencesmedicine.medical_specialtybusiness.industryEASDEndocrinology Diabetes and MetabolismHuman physiologymedicine.disease03 medical and health sciences0302 clinical medicineDiabetes mellitusFamily medicineInternal MedicineMedicinebusiness030217 neurology & neurosurgery030304 developmental biology
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The Friedreich's Ataxia protein frataxin modulates DNA base excision repair in prokaryotes and mammals

2010

DNA-repair mechanisms enable cells to maintain their genetic information by protecting it from mutations that may cause malignant growth. Recent evidence suggests that specific DNA-repair enzymes contain ISCs (iron–sulfur clusters). The nuclearencoded protein frataxin is essential for the mitochondrial biosynthesis of ISCs. Frataxin deficiency causes a neurodegenerative disorder named Friedreich's ataxia in humans. Various types of cancer occurring at young age are associated with this disease, and hence with frataxin deficiency. Mice carrying a hepatocyte-specific disruption of the frataxin gene develop multiple liver tumours for unresolved reasons. In the present study, we show that frata…

Iron-Sulfur ProteinsDNA Repairmedicine.disease_causeBiochemistryDNA Glycosylases8-oxoG 78-dihydro-8-oxoguanineMice0302 clinical medicineIron-Binding Proteinsoxidative stressBER base excision repairCells CulturedMammalsMice Knockout0303 health sciencesfrataxinDMEM Dulbecco's modified Eagle's mediumbiologyLiver NeoplasmsSalmonella entericairon–sulfur clusterLife SciencesIron-binding proteinsTransfection3. Good healthLB Luria–BertaniOGG1 8-oxoguanine DNA glycosylase 1ISC iron–sulfur clusterFpg formamido-pyrimidine DNA glycosylaseHPRT hypoxanthine phosphoribosyltransferaseResearch ArticleDNA damageDNA repairSSB DNA single-strand breakTransfectionCell Line03 medical and health sciencesFRDA Friedreich's ataxiaROS reactive oxygen speciesmedicineAnimalsHumansMUTYH human mutY homologue (Escherichia coli)Molecular BiologyGene030304 developmental biologyFriedreich's ataxiaCell BiologyFibroblastsMolecular biologytumorigenesisProkaryotic CellsFriedreich AtaxiaDNA base excision repairDNA glycosylaseMutationHepatocytesFrataxinbiology.proteinInstitut für ErnährungswissenschaftCarcinogenesisMAPK mitogen-activated protein kinase030217 neurology & neurosurgeryDNA Damage
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