Search results for "8-Hydroxy-2'-deoxyguanosine"

showing 10 items of 46 documents

Increased Oxidative Damage Associated with Unfavorable Cytogenetic Subgroups in Chronic Lymphocytic Leukemia

2014

Oxidative stress contributes to genomic instability in chronic lymphocytic leukemia (CLL), but its relationship with the acquisition of specific chromosomal abnormalities is unknown. We recruited 55 untreated CLL patients and assessed 8-oxo-2′-deoxyguanosine (8-oxo-dG), glutathione, and malondialdehyde (MDA) levels, and we compared them among the cytogenetic subgroups established using fluorescence in situ hybridization (FISH). Significant increases in 8-oxo-dG and/or MDA were observed in patients with unfavorable cytogenetic aberrations (17p and 11q deletions) compared to the 13q deletion group.TP53deletion patients exhibited a diminished DNA repair efficiency. Finally, cases with normal F…

MaleGenome instabilityArticle SubjectDNA RepairDNA damageDNA repairChronic lymphocytic leukemialcsh:MedicineBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCohort Studieschemistry.chemical_compoundMalondialdehydemedicineHumansLymphocytesIn Situ Hybridization FluorescenceAgedAged 80 and overChromosome AberrationsGeneral Immunology and Microbiologymedicine.diagnostic_testlcsh:RDeoxyguanosineGeneral MedicineGlutathioneMiddle AgedMalondialdehydemedicine.diseaseGlutathioneLeukemia Lymphocytic Chronic B-CellOxidative Stresschemistry8-Hydroxy-2'-DeoxyguanosineImmunologyFemaleLipid PeroxidationReactive Oxygen SpeciesGene DeletionOxidative stressDNA DamageResearch ArticleFluorescence in situ hybridizationBioMed Research International
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AZT induces oxidative damage to cardiac mitochondria: Protective effect of vitamins C and E

2004

Abstract AZT (zidovudine) is a potent inhibitor of HIV replication and a major antiretroviral drug used for AIDS treatment. A major limitation in the use of AZT is the occurrence of severe side effects. The aim of this work was to test whether AZT causes oxidative damage to heart mitochondria and whether this can be prevented by supranutritional doses of antioxidant vitamins. An experimental animal model was used in which mice were treated with AZT for 35 days (10 mg/kg/day) in drinking water. Animals treated with antioxidant vitamins were fed the same diet as controls but supplemented with vitamins C (ascorbic acid, 10 g/ kg diet) and E (α-dl-tocopherol, 0.6 g/kg diet) for 65 days before s…

MaleMitochondrial Diseasesmedicine.medical_treatmentAscorbic AcidOxidative phosphorylationMitochondrionPharmacologyBiologymedicine.disease_causeDNA MitochondrialMitochondria HeartGeneral Biochemistry Genetics and Molecular BiologyLipid peroxidationMiceZidovudinechemistry.chemical_compoundmedicineAnimalsVitamin Eheterocyclic compoundsGeneral Pharmacology Toxicology and PharmaceuticsVitamin CVitamin EDeoxyguanosineGeneral MedicineAscorbic acidGlutathioneBiochemistrychemistry8-Hydroxy-2'-DeoxyguanosineLipid PeroxidationZidovudineOxidative stressmedicine.drugLife Sciences
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Carcinogenic Etheno DNA Adducts in Alcoholic Liver Disease: Correlation with Cytochrome P-4502E1 and Fibrosis.

2017

BACKGROUND One mechanism by which alcoholic liver disease (ALD) progresses is oxidative stress and the generation of reactive oxygen species, among others due to the induction of cytochrome P-4502E1 (CYP2E1). Experimental data underline the key role of CYP2E1 because ALD could be partially prevented in rats by the administration of the specific CYP2E1 inhibitor chlormethiazole. As CYP2E1 is linked to the formation of carcinogenic etheno DNA adducts in ALD patients, a causal role of alcohol-induced CYP2E1 in hepatocarcinogenesis is implicated. The purpose of this study was to investigate CYP2E1 induction in ALD, and its correlation with oxidative DNA lesions and with hepatic histology. METHO…

Malemedicine.medical_specialtyAlcoholic liver diseaseCarcinoma HepatocellularCarcinogenesisMedicine (miscellaneous)Intra-Abdominal FatToxicologymedicine.disease_causeGastroenterology03 medical and health sciences0302 clinical medicineFibrosisLiver Cirrhosis AlcoholicInternal medicineDNA adductmedicineHumansLiver Diseases AlcoholicCarcinogenInflammationDeoxyadenosinesbusiness.industryLiver NeoplasmsDeoxyguanosineCytochrome P-450 CYP2E1CYP2E1Middle Agedmedicine.diseaseFibrosisImmunohistochemistryPsychiatry and Mental healthLiver8-Hydroxy-2'-Deoxyguanosine030220 oncology & carcinogenesis030211 gastroenterology & hepatologyFemaleSteatosisHepatic fibrosisbusinessOxidative stressAlcoholism, clinical and experimental research
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Human milk enhances antioxidant defenses against hydroxyl radical aggression in preterm infants

2008

Background: Preterm infants endowed with an immature antioxidant defense system are prone to oxidative stress. Hydroxyl radicals are very aggressive reactive oxygen species that lack specific antioxidants. These radicals cannot be measured directly, but oxidation byproducts of DNA or phenylalanine in urine are reliable markers of their activity. Human milk has a higher antioxidant capacity than formula. Objective: We hypothesized that oxidative stress associated with prematurity could be diminished by feeding human milk. Design: We recruited a cohort of stable preterm infants who lacked perinatal conditions associated with oxidative stress; were not receiving prooxidant or antioxidant drugs…

Malemedicine.medical_specialtyAntioxidantPhenylalaninemedicine.medical_treatmentMedicine (miscellaneous)Gestational AgePhenylalanineOxidative phosphorylationUrinemedicine.disease_causeAntioxidantsCohort StudiesTandem Mass SpectrometryInternal medicinemedicineHumansInfant Nutritional Physiological PhenomenaChromatography High Pressure Liquidchemistry.chemical_classificationAnalysis of VarianceReactive oxygen speciesNutrition and DieteticsMilk HumanHydroxyl RadicalInfant NewbornCase-control studyDeoxyguanosinemedicine.diseaseInfant FormulaOxidative StressEndocrinologychemistryBiochemistry8-Hydroxy-2'-DeoxyguanosinePremature birthCase-Control StudiesFemaleReactive Oxygen SpeciesBiomarkersInfant PrematureOxidative stressDNA DamageThe American Journal of Clinical Nutrition
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Antioxidant enzyme activities and the production of MDA and 8-oxo-dG in chronic lymphocytic leukemia.

2001

Abstract Chronic lymphocytic leukemia (CLL) is a neoplastic disease susceptible to antioxidant enzyme alterations and oxidative stress. We have examined the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), and the oxidized/reduced glutathione (GSSG/GSH) ratio together with the levels of malondialdehyde (MDA) and 8-oxo-2′-deoxyguanosine (8-oxo-dG) in lymphocytes of CLL patients and compared them with those of normal subjects of the same age. SOD and CAT activity decreased in CLL lymphocytes while GPx activity increased. GSH content of CLL lymphocytes also increased, and GSSG concentration remained constant. Thus, a reduced GSSG/GSH ratio was obtaine…

Malemedicine.medical_specialtyAntioxidantmedicine.medical_treatmentChronic lymphocytic leukemiamedicine.disease_causeBiochemistryAntioxidantsSuperoxide dismutasechemistry.chemical_compoundhemic and lymphatic diseasesPhysiology (medical)Internal medicineMalondialdehydemedicineHumansLymphocytesAgedchemistry.chemical_classificationGlutathione PeroxidasebiologySuperoxide DismutaseGlutathione peroxidaseDeoxyguanosineGlutathioneDNA NeoplasmMiddle AgedMalondialdehydemedicine.diseaseCatalaseGlutathioneLeukemia Lymphocytic Chronic B-CellEndocrinologychemistryBiochemistryCatalase8-Hydroxy-2'-Deoxyguanosinebiology.proteinFemaleLipid PeroxidationOxidoreductasesOxidative stressDNA DamageFree radical biologymedicine
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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
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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
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Protective effect of trehalose-loaded liposomes against UVB-induced photodamage in human keratinocytes

2014

Trehalose, a naturally occurring non-reducing disaccharide, is known to act as a major protein stabilizer that can reduce ultraviolet B (UVB)-induced corneal damage when topically applied to the eye. However, due to the low skin permeability of trehalose, which makes the development of topical formulations difficult, its use as a skin photoprotective agent has been limited. Previous findings demonstrated that liposomes may significantly improve the intracellular delivery of trehalose. Therefore, the present study aimed to assess the protective effects of trehalose-loaded liposomes against UVB-induced photodamage using the immortalized human keratinocyte cell line, HaCaT. The effects were al…

Ultraviolet radiationKeratinocytesCienciaPyrimidine dimerBiologyPharmacologyPhotoprotective agentGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundmedicineGeneral Pharmacology Toxicology and PharmaceuticsCiencias médicasLiposomeintegumentary systemGeneral NeurosciencePiel - InvestigaciónTrehaloseArticlesGeneral Medicinemedicine.diseaseTrehaloseProtein carbonylationCyclobutane pyrimidine dimersHaCaTchemistryApoptosisPhotoprotectionImmunology8-hydroxy-2'-deoxyguanosineSkin cancerBiomedical Reports
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alpha-Tocopherol, MDA-HNE and 8-OHdG levels in liver and heart mitochondria of adriamycin-treated rats fed with alcohol-free beer.

2008

Different studies indicate that oxidative stress and mitochondrial damage are key factors in different pathogenic process. The aim of this study was to investigate the possible protective role of alcohol-free beer on adriamycin-induced (ADR) heart and liver toxicity using biomarkers of oxidative stress. This effect was compared with the effect of alcohol beer intake and with a control group. Rats were randomly divided into six groups. The first group received no adriamycin, was fed with water and was regarded as the control group; the second group was injected with a ADR (two cycles of 5mg/kg); the third and fourth groups were fed with alcohol-free and beer for 21 days, respectively and the…

VitaminMalemedicine.medical_specialtyAntioxidantmedicine.medical_treatmentalpha-TocopherolAlcoholMitochondria LiverToxicologymedicine.disease_causeMitochondria Heartchemistry.chemical_compoundInternal medicineMalondialdehydemedicineAnimalsTocopherolRats WistarHeart metabolismAldehydesEthanolAntibiotics AntineoplasticEthanolfood and beveragesBeerCentral Nervous System DepressantsDeoxyguanosineProteinsMalondialdehydeLipid MetabolismRatsOxidative StressEndocrinologychemistryBiochemistry8-Hydroxy-2'-DeoxyguanosineDoxorubicinIndicators and ReagentsOxidative stressDNA DamageToxicology
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Vitamin A deficiency causes oxidative damage to liver mitochondria in rats.

2000

Mitochondrial damage in rat liver induced by chronic vitamin A-deficiency was studied using three different groups of rats: (i) control rats, (ii) rats fed a vitamin A-free diet until 50 d after birth and (iii) vitamin A-deficient rats re-fed a control diet for 30 d. No statistical difference in body weight and food intake was found between control and vitamin A-deficient rats. Liver GSH concentration was similar in both groups. However, in vitamin A-deficient rats, the mitochondrial GSH/GSSG ratio was significantly lower and the levels of malondialdehyde (MDA) and 8-oxo-7, 8-dihydro-2'-deoxyguanosine (oxo8dG) were higher when compared to control rats. These values were partially restored i…

Vitaminmedicine.medical_specialtyAgingPopulationMitochondria LiverBiologyMitochondrionmedicine.disease_causeWeight GainBiochemistryMembrane Potentialschemistry.chemical_compoundMembrane LipidsPhysiology (medical)Internal medicineMalondialdehydemedicineDeoxyguanosineAnimalseducationVitamin Aeducation.field_of_studyGlutathione DisulfideVitamin A DeficiencyDeoxyguanosineGlutathioneIntracellular Membranesmedicine.diseaseMalondialdehydeFlow CytometryGlutathioneRatsVitamin A deficiencyEndocrinologychemistry8-Hydroxy-2'-DeoxyguanosineFemaleEnergy IntakeOxidative stressFree radical biologymedicine
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