2011
Ultraviolet Radiation: Cellular Antioxidant Response and the Role of Ocular Aldehyde Dehydrogenase Enzymes
Marchitti SA, Chen Y, Thompson DC, Vasiliou V. Ultraviolet Radiation: Cellular Antioxidant Response and the Role of Ocular Aldehyde Dehydrogenase Enzymes. Eye & Contact Lens Science & Clinical Practice 2011, 37: 206-213. PMID: 21670692, PMCID: PMC3356694, DOI: 10.1097/icl.0b013e3182212642.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsReactive oxygen speciesCombat reactive oxygen speciesImportant enzymatic antioxidantsAldehyde dehydrogenaseReduction-oxidation homeostasisOxidative damageConstant oxidative stressAldehyde dehydrogenase enzymeCellular antioxidant responseOxidative stressUnique roleCellular membranesCellular responsesAntioxidant defense systemSuperoxide dismutasesAntioxidant responseEnvironmental insultsDownstream effectsDefense systemGlutathione reductaseEnzymatic antioxidantsOxygen speciesDehydrogenase enzymeNicotinamide adenine dinucleotide phosphateNonenzymatic antioxidants
2010
Glutathione deficient C57BL/6J mice are not sensitized to ozone-induced lung injury
Johansson E, Wesselkamper SC, Shertzer HG, Leikauf GD, Dalton TP, Chen Y. Glutathione deficient C57BL/6J mice are not sensitized to ozone-induced lung injury. Biochemical And Biophysical Research Communications 2010, 396: 407-412. PMID: 20417186, PMCID: PMC2892220, DOI: 10.1016/j.bbrc.2010.04.105.Peer-Reviewed Original ResearchConceptsOzone-induced lung injuryGlutamate-cysteine ligase modifier subunitLung injuryLung hyperpermeabilityDegree of neutrophiliaBronchoalveolar lavage fluidWild-type miceInflammatory gene expressionPulmonary susceptibilityLavage fluidCompensatory augmentationKnockout miceTotal protein concentrationPpm ozoneMiceModifier subunitMRNA levelsAntioxidant defenseMember 2Antioxidant glutathioneMetallothionein-1GSH depletionHyperpermeabilityInjuryAntioxidant response
2005
Butylhydroquinone Protects Cells Genetically Deficient in Glutathione Biosynthesis from Arsenite-Induced Apoptosis Without Significantly Changing Their Prooxidant Status
Kann S, Estes C, Reichard JF, Huang MY, Sartor MA, Schwemberger S, Chen Y, Dalton TP, Shertzer HG, Xia Y, Puga A. Butylhydroquinone Protects Cells Genetically Deficient in Glutathione Biosynthesis from Arsenite-Induced Apoptosis Without Significantly Changing Their Prooxidant Status. Toxicological Sciences 2005, 87: 365-384. PMID: 16014739, DOI: 10.1093/toxsci/kfi253.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisArsenitesBlotting, WesternCell SurvivalCells, CulturedDNA, ComplementaryElectrophoretic Mobility Shift AssayFibroblastsGene Expression RegulationGlutamate-Cysteine LigaseGlutathioneHydroquinonesMiceMice, KnockoutNF-kappa BOligonucleotide Array Sequence AnalysisOxidantsOxidative StressRNATetrazolium SaltsThiazolesConceptsMouse embryo fibroblastsGlutathione biosynthesisGlobal gene expression profilesAntioxidant responseCell cycle regulationArsenite-induced apoptosisEffective antioxidant responseArsenic-induced apoptosisGene expression profilesExpression of genesGlutamate-cysteine ligaseOxidative stressProtein biosynthesisRole of glutathioneCycle regulationRate-limiting enzymeGene deregulationExpression profilesArsenic-induced oxidative stressEmbryo fibroblastsInduces oxidative stressModifier subunitApoptotic deathDNA damageToxicity of arsenic