Search results for "Redox regulation"

showing 4 items of 4 documents

The Expression of NOX From Synthetic Promoters Reveals an Important Role of the Redox Status in Regulating Secondary Metabolism of

2020

Redox cofactors play a pivotal role in primary cellular metabolism, whereas the clear link between redox status and secondary metabolism is still vague. In this study we investigated effects of redox perturbation on the production of erythromycin in Saccharopolyspora erythraea by expressing the water-forming NADH oxidase (NOX) from Streptococcus pneumonia at different levels with synthetic promoters. The expression of NOX reduced the intracellular [NADH]/[NAD+] ratio significantly in S. erythraea which resulted in an increased production of erythromycin by 19∼29% and this increment rose to 60% as more oxygen was supplied. In contrast, the lower redox ratio resulted in a decreased production…

0301 basic medicineHistologylcsh:BiotechnologyBiomedical EngineeringBioengineering02 engineering and technologyRedoxCofactorredox regulation03 medical and health scienceschemistry.chemical_compoundBiosynthesislcsh:TP248.13-248.65Guanosine monophosphateSecondary metabolismOriginal Researchsecondary metabolismbiologyBioengineering and Biotechnologyc-di-GMP021001 nanoscience & nanotechnologybiology.organism_classificationSaccharopolyspora erythraea030104 developmental biologysynthetic promotersBiochemistrychemistryNADH oxidasebiology.proteinDiguanylate cyclaseSaccharopolyspora erythraeaNAD+ kinase0210 nano-technologyBiotechnologyFrontiers in bioengineering and biotechnology
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Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species

2010

This review highlights the important role of redox signaling between mitochondria and NADPH oxidases. Besides the definition and general importance of redox signaling, the cross-talk between mitochondrial and Nox-derived reactive oxygen species (ROS) is discussed on the basis of 4 different examples. In the first model, angiotensin-II is discussed as a trigger for NADPH oxidase activation with subsequent ROS-dependent opening of mitochondrial ATP-sensitive potassium channels leading to depolarization of mitochondrial membrane potential followed by mitochondrial ROS formation and respiratory dysfunction. This concept was supported by observations that ethidium bromide-induced mitochondrial d…

Mitochondrial ROSAgingPotassium ChannelsMyocytes Smooth MuscleBiophysicsIn Vitro TechniquesMitochondrionmedicine.disease_causeMitochondrial Membrane Transport ProteinsModels BiologicalMitochondrial apoptosis-induced channelBiochemistryPeroxynitritechemistry.chemical_compoundmedicineAnimalsHumansMitochondrionFeedback PhysiologicalNADPH oxidasebiologyNADPH oxidaseMitochondrial Permeability Transition PoreSuperoxideAngiotensin IINADPH OxidasesSuperoxideNitric oxideCell BiologyReactive Nitrogen SpeciesMitochondriaCell biologyOxidative StressOxidative protein modificationchemistryMitochondrial permeability transition poreRedox regulationNOX1Hypertensionbiology.proteinReactive Oxygen SpeciesOxidation-ReductionOxidative stressSignal TransductionBiochimica et Biophysica Acta (BBA) - Bioenergetics
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Redox Regulation of Metabolic Syndrome: From Biochemical Mechanisms to Nutritional Interventions.

2021

According to its “harmonized” definition, metabolic syndrome (MetS) is described as a cluster of metabolic factors that increases the risk of cardiovascular diseases, diabetes (DM) and associated morbidities such as dementia [...]

Physiologybusiness.industryClinical BiochemistryMEDLINECell BiologyRM1-950medicine.diseaseBioinformaticsDisease clusterBiochemistrymetabolic syndromeredox regulationn/aEditorialNutritional InterventionsDiabetes mellitusmental disordersmedicineDementiaTherapeutics. PharmacologyMetabolic syndromebusinessMolecular BiologyAntioxidants (Basel, Switzerland)
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Prolonging in utero-like oxygenation after birth diminishes oxidative stress in the lung and brain of mice pups☆

2013

Background Fetal-to-neonatal transition is associated with oxidative stress. In preterm infants, immaturity of the antioxidant system favours supplemental oxygen-derived morbidity and mortality. Objectives To assess if prolonging in utero-like oxygenation during the fetal-to-neonatal transition limits oxidative stress in the lung and brain, improving postnatal adaptation of mice pups. Material and methods Inspiratory oxygen fraction (FiO2) in pregnant mice was reduced from 21% (room air) to 14% (hypoxia) 8–12 h prior to delivery and reset to 21% 6–8 h after birth. The control group was kept at 21% during the procedure. Reduced (GSH) and oxidized (GSSG) glutathione and its precursors [γ-glut…

gsr (glutathione reductase gene)pgd phosphogluconate dehydrogenase geneGPX1FiO2 inspiratory oxygen fractionγ-GC (gamma-glutamyl cysteine)PhysiologyBiochemistryMice0302 clinical medicinePregnancyquinone oxidoreductase 1) [noq1 (NAD(P)H]NAD(P)H Dehydrogenase (Quinone)gapdh glyceraldehyde-3-phosphate dehydrogenase geneP7 1 week after birthGSH (reduced glutathione)Oxidoreductases Acting on Sulfur Group Donorsme1 (malic enzyme 1 gene)glutathioneLungSpO2 oxygen saturationlcsh:QH301-705.5γ-GC–NEM gamma-glutamyl cysteine covalently bonded to N-ethylmaleimidechemistry.chemical_classification0303 health sciencesGSSG oxidized glutathioneGlutathione peroxidaseO14 (hypoxia group FiO2=14%)Brainm/z mass-to-charge ratioG18 18th day of gestationCell Hypoxia3. Good healthpgd (phosphogluconate dehydrogenase gene)In uterogclm glutamylcysteine ligase modifier subunit genesrnx1 sulfiredoxin 1 genelcsh:Medicine (General)me1 malic enzyme 1 genesrnx1 (sulfiredoxin 1 gene)gclm (glutamylcysteine ligase modifier subunit gene)γ-GC–NEM (gamma-glutamyl cysteine covalently bonded to N-ethylmaleimide)trxnd1 (thioredoxin reductase 1 gene)redox regulation03 medical and health sciencesnoq1 NAD(P)H:quinone oxidoreductase 1γ-GC gamma-glutamyl cysteineCySH L-cysteinePregnancyg6pdx (glucose 6 phosphate dehydrogenase gene)GlutathioneOxygenationgapdh (glyceraldehyde-3-phosphate dehydrogenase gene)medicine.diseaseMice Inbred C57BLOxygenP1 24 h after birthGCL glutamylcysteine ligasechemistryOxidative stressRedox regulationNEM (N-ethylmaleimide)O14 hypoxia group (FiO2=14%)GSH reduced glutathioneClinical Biochemistrymedicine.disease_causechemistry.chemical_compoundGlutathione Peroxidase GPX1GS–NEM reduced glutathione covalently bonded to N-ethylmaleimideSpO2 (oxygen saturation)oxidative stressg6pdx glucose 6 phosphate dehydrogenase genelcsh:R5-920GSSG (oxidized glutathione)G18 (18th day of gestation)gsr glutathione reductase geneGlutathionegpx1 glutathione peroxidase 1 genemedicine.anatomical_structurem/z (mass-to-charge ratio)LC–MS/MS (liquid chromatography coupled to tandem mass spectrometry)FemaleLC–MS/MS liquid chromatography coupled to tandem mass spectrometryO21 (normoxia group FiO2=21%)paO2 (partial pressure of oxygen)gpx1 (glutathione peroxidase 1 gene)Research Papernoq1 (NAD(P)H:quinone oxidoreductase 1)CySH (l-cysteine)FiO2 (inspiratory oxygen fraction)CyS–NEM (cysteine covalently bonded to N-ethylmaleimide)030225 pediatricsmedicineP7 (1 week after birth)AnimalsGCL (glutamylcysteine ligase)P1 (24 h after birth)O21 normoxia group (FiO2=21%)CyS–NEM cysteine covalently bonded to N-ethylmaleimide030304 developmental biologyGlutathione PeroxidaseLungOrganic ChemistryGS–NEM (reduced glutathione covalently bonded to N-ethylmaleimide)trxnd1 thioredoxin reductase 1 geneMolecular biologypaO2 partial pressure of oxygenAnimals NewbornGene Expression Regulationlcsh:Biology (General)NEM N-ethylmaleimidefetal-to-neonatal transitionoxygenOxidative stressFetal-to-neonatal transition
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