Search results for "Oxidation-Reduction"

showing 10 items of 689 documents

Ursodeoxycholic acid protects against secondary biliary cirrhosis in rats by preventing mitochondrial oxidative stress

2004

Ursodeoxycholic acid (UDCA) improves clinical and biochemical indices in primary biliary cirrhosis and prolongs survival free of liver transplantation. Recently, it was suggested that the cytoprotective mechanisms of UDCA may be mediated by protection against oxidative stress, which is involved in the development of cirrhosis induced by chronic cholestasis. The aims of the current study were 1) to identify the mechanisms involved in glutathione depletion, oxidative stress, and mitochondrial impairment during biliary cirrhosis induced by chronic cholestasis in rats; and 2) to determine the mechanisms associated with the protective effects of UDCA against secondary biliary cirrhosis. The find…

Malemedicine.medical_specialtyCirrhosisCardiolipinsGlutamate-Cysteine LigaseBiliary cirrhosisPopulationBiologymedicine.disease_causeMembrane Potentialschemistry.chemical_compoundPrimary biliary cirrhosisInternal medicinemedicineCardiolipinAnimalsRats Wistareducationeducation.field_of_studyCholestasisHepatologyLiver Cirrhosis BiliaryUrsodeoxycholic AcidCystathionine gamma-LyaseGlutathionemedicine.diseaseGlutathioneUrsodeoxycholic acidMitochondriaPeroxidesRatsOxidative StressEndocrinologyLiverchemistryChronic DiseaseHepatocytesOxidation-ReductionOxidative stressmedicine.drugHepatology
researchProduct

Effects of insulin-like growth factor I on the rates of glucose transport and utilization in rat skeletal muscle in vitro.

1992

1. The effects of insulin-like growth factor I (IGF-I) on the rates of glucose transport and utilization and its interaction with insulin were investigated in rat soleus muscle in vitro. IGF-I increased the rates of glucose transport, lactate formation, glycogen synthesis and the flux of glucose to hexose monophosphate, but it had no effect on the rate of glucose oxidation or glycogenolysis. 2. In the absence of insulin, low levels of IGF-I (0-30 ng/ml) increased the rate of glycolysis and the content of fructose 2,6-bisphosphate, but the content of glucose 6-phosphate remained unaltered; at higher levels of IGF-I (300-3000 ng/ml) the rate of glycolysis and the content of fructose 2,6-bisph…

Malemedicine.medical_specialtyGlycogenolysismedicine.medical_treatmentGlucose-6-PhosphateBiologyIn Vitro TechniquesBiochemistrychemistry.chemical_compoundInternal medicinemedicineFructosediphosphatesAnimalsInsulinGlycolysisInsulin-Like Growth Factor IPhosphorylationGlycogen synthaseMolecular BiologyGlycogenInsulinMusclesGlucose transporterGlucosephosphatesFructoseBiological TransportRats Inbred StrainsCell BiologyRatsKineticsEndocrinologyGlucosechemistryFructolysisbiology.proteinGlycolysisOxidation-ReductionGlycogenResearch Article
researchProduct

Studies on the disposition, metabolism and hepatotoxicity of coumarin in the rat and Syrian hamster.

2002

The hepatotoxicity, metabolism and disposition of coumarin has been compared in male Sprague-Dawley rats and Syrian hamsters. The treatment of rats for 12, 24 and 42 weeks with diets containing 0.2 and 0.5% coumarin resulted in hepatotoxicity and increased relative liver weights. While levels of cytochrome P450 (CYP) and CYP-dependent enzymes were decreased, levels of reduced glutathione (GSH) and activities of UDP glucuronosyltransferase, gamma-glutamyltransferase and GSH S-transferase were increased. In contrast, coumarin produced few hepatic changes in the Syrian hamster. Following a single oral dose of 25 mg/kg [3-14C]coumarin, radioactivity was rapidly excreted by the rat and Syrian ha…

Malemedicine.medical_specialtyHamsterToxicologyRats Sprague-Dawleychemistry.chemical_compoundCytosolPharmacokineticsLiver Function TestsSpecies SpecificityOral administrationCoumarinsInternal medicineCricetinaemedicineToxicokineticsAnimalsheterocyclic compoundsTissue DistributionNutritionbiologyMesocricetusBody WeightCytochrome P450AnticoagulantsGeneral MedicineGlutathioneOrgan SizeCoumarinGlutathioneDietRatsEndocrinologychemistryLiverToxicitybiology.proteinChemical and Drug Induced Liver InjuryOxidation-ReductionFood ScienceFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
researchProduct

The aminothiol redox status in haemodialysis patients does not improve with folate therapy.

2008

Patients on haemodialysis suffer from high cardiovascular morbidity and mortality, and oxidative stress may play a role in the pathophysiology of cardiovascular disease in these patients. Hyperhomocysteinemia is common in dialysis patients and may have pro-oxidant effects. Moreover, the redox status of the major plasma aminothiols (homocysteine [Hcy], cysteine and cysteinylglycine) may be regarded as a biomarker of oxidative stress. In the present study, we investigated the aminothiol redox status during a period of homocysteine-lowering therapy with folinic acid.In the first part of the study, 32 stable patients receiving maintenance haemodialysis were compared with 32 reference subjects. …

Malemedicine.medical_specialtyHyperhomocysteinemiaHomocysteineClinical Biochemistrymedicine.disease_causeGastroenterologychemistry.chemical_compoundFolinic acidFolic AcidRenal DialysisInternal medicinemedicineHumansSulfhydryl CompoundsAgedbusiness.industryGeneral MedicineMiddle Agedmedicine.diseaseRedox statusPathophysiologySurgerychemistryBiomarker (medicine)FemalebusinessOxidation-ReductionOxidative stressCysteinemedicine.drugScandinavian journal of clinical and laboratory investigation
researchProduct

Hepatic steatosis is not due to impaired fatty acid oxidation capacities in C57BL/6J mice fed the conjugated trans-10,cis-12-isomer of linoleic acid.

2004

Decreased body fat mass and liver steatosis have been reported in mice fed diets containing the conjugated linoleic acid trans-10,cis-12-C18:2 (CLA2), but not in those fed diets containing cis-9,trans-11-C18:2 (CLA1). Because the decrease in fatty acid (FA) oxidation may cause fat accumulation, we questioned whether the effects of both CLAs on enzyme activities and mRNA expression were related to liver FA oxidation. To address this question, 7-wk-old male C57BL/6J mice were fed for 4 wk a diet supplemented with 1% CLA1, CLA2, or cis-9-C18:1 (control) esterified as triacylglycerols. In CLA2-fed mice, the proportions of CLA2 in the total FA of liver lipids were substantially lower than those …

Malemedicine.medical_specialtyLinoleic acidConjugated linoleic acidMedicine (miscellaneous)Mitochondria LiverBiologychemistry.chemical_compoundMiceDietary Fats UnsaturatedInternal medicinemedicineAnimalsLinoleic Acids ConjugatedCarnitineRNA MessengerEnzyme InhibitorsUnsaturated fatty acidTriglycerideschemistry.chemical_classificationNutrition and DieteticsCarnitine O-PalmitoyltransferaseEsterificationReverse Transcriptase Polymerase Chain ReactionFatty liverFatty AcidsFatty acidmedicine.diseaseFatty LiverMalonyl Coenzyme AMice Inbred C57BLEndocrinologychemistryBiochemistryLiverCarnitine palmitoyltransferase IOxidation-ReductionPolyunsaturated fatty acidmedicine.drug
researchProduct

Changes in brain oxidative metabolism induced by inhibitory avoidance learning and acute administration of amitriptyline

2007

The effects of antidepressant drugs on memory have been somewhat ignored, having been considered a mere side effect of these compounds. However, the memory impairment caused by several antidepressants could be considered to form part of their therapeutic effects. Amitriptyline is currently one of the most prescribed tricyclic antidepressants, and exerts marked anticholinergic and antihistaminergic effects. In this study, we evaluated the effects of inhibitory avoidance (IA) learning and acute administration of amitriptyline on brain oxidative metabolism. Brain oxidative metabolism was measured in several limbic regions using cytochrome oxidase (CO) quantitative histochemistry. Amitriptyline…

Malemedicine.medical_specialtyMammillary bodyAmitriptylineClinical BiochemistryInfralimbic cortexCentral nervous systemAntidepressive Agents TricyclicToxicologyBiochemistryElectron Transport Complex IVMiceBehavioral NeuroscienceLimbic systemInternal medicineAvoidance LearningAnimalsMedicineAmitriptylinePrefrontal cortexBiological PsychiatryPharmacologybusiness.industryDentate gyrusBrainDiagonal band of Brocamedicine.anatomical_structureEndocrinologybusinessOxidation-Reductionmedicine.drugPharmacology Biochemistry and Behavior
researchProduct

Late onset administration of oral antioxidants prevents age-related loss of motor co-ordination and brain mitochondrial DNA damage.

1999

We have studied the effect of aging on brain glutathione redox ratio, on brain mitochondrial DNA damage and on motor co-ordination in mice and the possible protective role of late onset administration of sulphur-containing antioxidants. Glutathione redox ratios change to a more oxidized state in whole brain with aging but the changes are much more pronounced when this ratio is measured in brain mitochondria. The levels of 8-oxo-7,8-dihydro-2 '-deoxyguanosine in mitochondrial DNA are much higher in the brain of old animals than in those of young ones. Late onset oral administration of sulphur-containing antioxidants partially prevents oxidation of mitochondrial glutathione and DNA. There is …

Malemedicine.medical_specialtyMitochondrial DNAAgingAdministration OralLate onsetMice Inbred StrainsBiologyMotor Activitymedicine.disease_causeBiochemistryRedoxDNA MitochondrialAntioxidantsDrug Administration Schedulechemistry.chemical_compoundMiceOral administrationInternal medicineAge relatedmedicineAnimalsPostural BalanceAlanineBrainDeoxyguanosineGeneral MedicineGlutathioneMolecular biologyGlutathioneThiazolesEndocrinologychemistry8-Hydroxy-2'-DeoxyguanosineOxidation-ReductionOxidative stressDNASulfurDNA DamageFree radical research
researchProduct

Mitochondrial glutathione oxidation correlates with age-associated oxidative damage to mitochondrial DNA

1996

Mitochondria may be primary targets of free radical damage associated with aging. We have found that mitochondrial glutathione is markedly oxidized with aging in rats and mice. The oxidized to reduced glutathione ratio rises with aging in the liver, kidney, and brain. The magnitude of these changes is much higher than that previously found in whole cells of any species previously studied. In the liver, this ratio (expressing GSSG as a percent of GSH) changed from 0.77 +/- 0.19% (n=5) in young rats to 2.47 +/- 1.25% (n=5) in old ones, i.e., 320% of the controls. In the brain and kidney, values for old rats were, respectively, 600 and 540% higher than those of young rats. A marked oxidation o…

Malemedicine.medical_specialtyMitochondrial DNAAgingAntioxidantmedicine.medical_treatmentMitochondrionmedicine.disease_causeBiochemistryDNA MitochondrialAntioxidantschemistry.chemical_compoundMiceInternal medicineGeneticsmedicineDeoxyguanosineAnimalsRats WistarMolecular BiologyFree-radical theory of agingKidneyGlutathione DisulfideChemistryDeoxyguanosineGlutathioneGlutathioneRatsMice Inbred C57BLOxidative StressEndocrinologymedicine.anatomical_structure8-Hydroxy-2'-DeoxyguanosineRabbitsOxidation-ReductionOxidative stressBiotechnologyDNA Damage
researchProduct

The Effect of Indobufen on the Activities of Selected Rat Liver Phase I and Phase II Drug Metabolizing Enzymes, Peroxisomal β-oxidation and Hepatic G…

1994

Abstract Oral administration of indobufen to male rats for three days at daily doses of 5, 10 and 20 mg kg−1 resulted in no changes in liver total glutathione, cytosolic glutathione S-transferases or microsomal epoxide hydrolase. Reduced glutathione appeared slightly diminished to about 84% of control at the highest dose level. Microsomal cytochrome P450-dependent ethoxyresorufin O-de-ethylase and pentoxyresorufin de-alkylase activities were decreased to 64% (not significantly) and 67% of control at the lowest dose level. 6α- and 7α-Hydroxytestosterone activities were decreased to 67 and 68% of control at the highest dose level. Cyanide-insensitive peroxisomal fatty acid β-oxidation was inc…

Malemedicine.medical_specialtyPharmaceutical ScienceIsoindolesBiologyMicrobodieschemistry.chemical_compoundCytochrome P-450 Enzyme SystemOral administrationInternal medicinemedicineAnimalsGlutathione TransferaseEpoxide HydrolasesPharmacologychemistry.chemical_classificationIndobufenDose-Response Relationship DrugFatty AcidsFatty acidCytochrome P450Rats Inbred StrainsGlutathionePeroxisomeGlutathionePhenylbutyratesRatsEndocrinologyLiverchemistryMicrosomal epoxide hydrolaseMicrosomebiology.proteinOxidation-Reductionmedicine.drugJournal of Pharmacy and Pharmacology
researchProduct

Paracrine Activation of Hepatic CB1 Receptors by Stellate Cell-Derived Endocannabinoids Mediates Alcoholic Fatty Liver

2008

SummaryAlcohol-induced fatty liver, a major cause of morbidity, has been attributed to enhanced hepatic lipogenesis and decreased fat clearance of unknown mechanism. Here we report that the steatosis induced in mice by a low-fat, liquid ethanol diet is attenuated by concurrent blockade of cannabinoid CB1 receptors. Global or hepatocyte-specific CB1 knockout mice are resistant to ethanol-induced steatosis and increases in lipogenic gene expression and have increased carnitine palmitoyltransferase 1 activity, which, unlike in controls, is not reduced by ethanol treatment. Ethanol feeding increases the hepatic expression of CB1 receptors and upregulates the endocannabinoid 2-arachidonoylglycer…

Malemedicine.medical_specialtyPhysiologyHUMDISEASEArachidonic AcidsGlyceridesMiceCarnitine palmitoyltransferase 1PiperidinesReceptor Cannabinoid CB1Internal medicineCannabinoid Receptor ModulatorsParacrine CommunicationmedicineAnimalsReceptorDiet Fat-RestrictedMolecular BiologyCells CulturedMice KnockoutCarnitine O-PalmitoyltransferaseEthanolChemistryLipogenesisFatty AcidsFatty liverCell Biologymedicine.diseaseEndocannabinoid systemCoculture TechniquesUp-RegulationMice Inbred C57BLDisease Models AnimalLipoprotein LipaseEndocrinologyLiverLipogenesisHepatocytesHepatic stellate cellPyrazoleslipids (amino acids peptides and proteins)Alcoholic fatty liverFatty Acid SynthasesRimonabantSteatosisSterol Regulatory Element Binding Protein 1Oxidation-ReductionEndocannabinoidsFatty Liver AlcoholicCell Metabolism
researchProduct