2021
Identification of Dose-Dependent DNA Damage and Repair Responses From Subchronic Exposure to 1,4-Dioxane in Mice Using a Systems Analysis Approach
Charkoftaki G, Golla JP, Santos-Neto A, Orlicky DJ, Garcia-Milian R, Chen Y, Rattray NJW, Cai Y, Wang Y, Shearn CT, Mironova V, Wang Y, Johnson CH, Thompson DC, Vasiliou V. Identification of Dose-Dependent DNA Damage and Repair Responses From Subchronic Exposure to 1,4-Dioxane in Mice Using a Systems Analysis Approach. Toxicological Sciences 2021, 183: 338-351. PMID: 33693819, PMCID: PMC8921626, DOI: 10.1093/toxsci/kfab030.Peer-Reviewed Original ResearchConceptsDX exposureBile acid quantificationRepair responseBDF-1 miceDNA damageDose-dependent DNA damageEffects of exposureHistopathological studySubchronic exposureImmunohistochemical analysisLiver carcinogenLiver carcinogenicityLiver transcriptomicsDrinking waterMetabolomic profilingMicePotential mechanismsLiverEnvironmental chemicalsState maximum contaminant levelToxic effectsCell deathExposureOxidative stress responsePresent study
2012
Molecular mechanisms of ALDH3A1-mediated cellular protection against 4-hydroxy-2-nonenal
Black W, Chen Y, Matsumoto A, Thompson DC, Lassen N, Pappa A, Vasiliou V. Molecular mechanisms of ALDH3A1-mediated cellular protection against 4-hydroxy-2-nonenal. Free Radical Biology And Medicine 2012, 52: 1937-1944. PMID: 22406320, PMCID: PMC3457646, DOI: 10.1016/j.freeradbiomed.2012.02.050.Peer-Reviewed Original ResearchConceptsAldehyde dehydrogenasesOxidative stress responseCellular defense mechanismsOxidative stressHuman ALDH3A1Proteasome functionMolecular mechanismsPrevents apoptosisStress responseCellular protectionLipid peroxidationAdverse effectsWestern blot analysisAldehydic moleculesGlutathione homeostasisALDH3A1 expressionCell viability assaysMetabolic functionsALDH3A1Blot analysisDefense mechanismsProtein adduct formationCell linesCell viabilityViability assays
2011
Lipid metabolism and body composition in Gclm(−/−) mice
Kendig EL, Chen Y, Krishan M, Johansson E, Schneider SN, Genter MB, Nebert DW, Shertzer HG. Lipid metabolism and body composition in Gclm(−/−) mice. Toxicology And Applied Pharmacology 2011, 257: 338-348. PMID: 21967773, PMCID: PMC3226854, DOI: 10.1016/j.taap.2011.09.017.Peer-Reviewed Original ResearchConceptsHigh-fat dietExcessive weight gainInsulin resistanceWeight gainFatty liverBasal metabolic rateGlutamate-cysteine ligase modifier subunit geneDecreased respiratory quotientExcess body weightIntestinal lipid absorptionHepatic oxidative stress responseDietary energy consumptionWild-type controlsGlucose intoleranceOxidative stress responseFat dietNormal dietRisk factorsBody compositionBody weightMetabolic rateDietary lipidsLipid absorptionMetabolic diseasesExperimental animals
2002
Initial Characterization of the Glutamate-Cysteine Ligase Modifier Subunit Gclm(−/−) Knockout Mouse NOVEL MODEL SYSTEM FOR A SEVERELY COMPROMISED OXIDATIVE STRESS RESPONSE*
Yang Y, Dieter MZ, Chen Y, Shertzer HG, Nebert DW, Dalton TP. Initial Characterization of the Glutamate-Cysteine Ligase Modifier Subunit Gclm(−/−) Knockout Mouse NOVEL MODEL SYSTEM FOR A SEVERELY COMPROMISED OXIDATIVE STRESS RESPONSE*. Journal Of Biological Chemistry 2002, 277: 49446-49452. PMID: 12384496, DOI: 10.1074/jbc.m209372200.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAllelesAnimalsBlotting, NorthernBlotting, SouthernBody WeightCell DeathChromatography, GelCysteineDose-Response Relationship, DrugFibroblastsGenotypeGlutamate-Cysteine LigaseGlutamic AcidGlutathioneHomozygoteHydrogen PeroxideImmunoblottingKidneyKineticsLiverMiceMice, KnockoutModels, GeneticMutagenesis, Site-DirectedOxidative StressOxygenPhenotypePolymerase Chain ReactionProtein Structure, TertiaryTime FactorsTissue DistributionConceptsGlutamate-cysteine ligaseModifier subunitGSH biosynthesis pathwayGlutamate-cysteine ligase modifier subunitOxidative stress responseGCL holoenzymeHigher eukaryotesBiosynthesis pathwayCellular functionsCatalytic subunitNovel model systemRate-limiting enzymeNumerous pathophysiological conditionsNull allelesStress responseOvert phenotypeGCL activityOxidant insultSubunitsFetal fibroblastsChronic GSH depletionInitial characterizationHoloenzymeGSH inhibitionGSH depletion