Search results for "toxicity."

showing 10 items of 2180 documents

Cytotoxicity of oleanolic and ursolic acid derivatives toward hepatocellular carcinoma and evaluation of NF-κB involvement.

2019

Oleanolic and ursolic acids are two ubiquitous isomeric triterpene phytochemicals known for their anticancer activity. A set of derivatives of the two compounds with a modified oxidation state and lipophylicity at C-3 and C-28 positions, were prepared and tested as anticancer agents versus the lines HepG2, Hep3B and HA22T/VGH of hepatocarcinoma, a strongly aggressive tumor that is not responsive toward the standard therapies. New derivatives containing a three carbons side chain on the C-3 position were synthetized in both stereoisomeric forms by the Barbier-Grignard procedure and three of them were found to be active toward all of the three targets. The implication of the transcriptional n…

Carcinoma HepatocellularApoptosis01 natural sciencesBiochemistrychemistry.chemical_compoundUrsolic acid Oleanolic acid HepG2 Hep3B HA22T/VGH Antitumor activity NF−κBUrsolic acidTriterpeneOleaDrug DiscoverymedicineTumor Cells CulturedHumansSettore BIO/15 - Biologia FarmaceuticaOleanolic AcidCytotoxicityMolecular BiologyCell Proliferationchemistry.chemical_classification010405 organic chemistryPlant ExtractsOrganic ChemistryLiver NeoplasmsNF-kappa BNF-κBSettore CHIM/06 - Chimica Organicamedicine.diseaseAntineoplastic Agents Phytogenicdigestive system diseasesTriterpenes0104 chemical sciences010404 medicinal & biomolecular chemistrychemistryMechanism of actionHepatocellular carcinomaMalusSettore BIO/14 - FarmacologiaCancer researchmedicine.symptomBioorganic chemistry
researchProduct

Use of HepG2 cell line for direct or indirect mutagens screening: comparative investigation between comet and micronucleus assays.

2003

International audience; In the present study, DNA-damage and clastogenic or aneugenic effects of genotoxic compounds were examined in a metabolically competent human cell line (HepG2 cells) using the micronucleus and the comet assays. Compounds with various action mechanisms were tested: direct mutagens such as 4-nitroquinoline-N-oxide (4-NQO) and methyl methanesulfonate (MMS) and indirect mutagens requiring biotransformation to be active such as N-nitrosodimethylamine (NDMA), benzo[a]pyrene (B[a]P) and 2-acetylaminofluorene (2-AAF). The compounds were first tested for cytotoxicity by measuring their effects on RNA synthesis inhibition in HepG2 cells. 4-NQO, B[a]P and 2-AAF were the most po…

Carcinoma HepatocellularNitrosaminesHealth Toxicology and Mutagenesis[SDV]Life Sciences [q-bio]Mutagen[SDV.TOX.TCA]Life Sciences [q-bio]/Toxicology/Toxicology and food chain010501 environmental sciencesQuinolonesmedicine.disease_cause01 natural sciencesSensitivity and SpecificityDimethylnitrosamine03 medical and health sciencesClastogenchemistry.chemical_compoundInhibitory Concentration 50GeneticsmedicineBenzo(a)pyreneTumor Cells CulturedHumansCytotoxicityComputingMilieux_MISCELLANEOUS030304 developmental biology0105 earth and related environmental sciencesGenetics0303 health sciencesMicronucleus TestsChemistryLiver Neoplasms2-AcetylaminofluoreneMethyl MethanesulfonateMolecular biology4-Nitroquinoline-1-oxideMethyl methanesulfonateComet assay[SDV] Life Sciences [q-bio]Micronucleus testComet AssayMicronucleusGenotoxicityMutagensMutation research
researchProduct

Toxicity of waste gasification bottom ash leachate

2011

Abstract Toxicity of waste gasification bottom ash leachate from landfill lysimeters (112 m3) was studied over three years. The leachate of grate incineration bottom ash from a parallel setup was used as reference material. Three aquatic organisms (bioluminescent bacteria, green algae and water flea) were used to study acute toxicity. In addition, an ethoxyresorufin-O-deethylase (EROD) assay was performed with mouse hepatoma cells to indicate the presence of organic contaminants. Concentrations of 14 elements and 15 PAH compounds were determined to characterise leachate. Gasification ash leachate had a high pH (9.2–12.4) and assays with and without pH adjustment to neutral were used. Gasifi…

Carcinoma Hepatocellularanimal diseasesta1172Coal AshMiceAlgaeChlorophytaToxicity TestsCytochrome P-450 CYP1A1Tumor Cells CulturedAnimalsLeachateWaste Management and DisposalWaste managementbiologyChemistryLiver Neoplasmstechnology industry and agricultureContaminationbiology.organism_classificationAliivibrio fischeriAcute toxicityRefuse DisposalIncinerationEnzyme ActivationDaphniaBottom ashLysimeterEnvironmental chemistryLuminescent MeasurementsGreen algaeWater Pollutants ChemicalWaste Management
researchProduct

Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardioto…

2015

Although treatment for heart failure induced by cancer therapy has improved in recent years, the prevalence of cardiomyopathy due to antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in cancer patients. The development of novel protective therapies requires testing putative therapeutic strategies in appropriate animal model…

Cardiac function curveACE inhibitorsCardiotonic AgentsNeuregulin-1CardiomyopathyAntineoplastic AgentsPreclinical modelsCardioprotectionCardiotonic AgentsPharmacologyBioinformaticsmedicine.disease_causeCancer therapy-induced cardiac injury ;Preclinical modelsMitochondria HeartBeta-blockersNeoplasmsCancer therapy-induced cardiac injuryMedicineAnimalsHumansCardiac stem cellsCardioprotectionCardiotoxicityACE inhibitors; Beta-blockers; Cancer therapy-induced cardiac injury; Cardiac stem cells; Cardioprotection; Mitochondria; Neuregulin-1; Oxidative stress; Preclinical models; Statinsbusiness.industryStatinsCancermedicine.diseaseCardiotoxicityMitochondriaCancer therapy-induced cardiac injury Preclinical models Cardioprotection Mitochondria Neuregulin-1 Oxidative stress Statins Beta-blockers ACE inhibitors Cardiac stem cellsDisease Models AnimalOxidative StressHeart failureCardiology and Cardiovascular MedicinebusinessOxidative stress
researchProduct

Chemotherapy cardiotoxicity: cardioprotective drugs and early identification of cardiac dysfunction.

2016

Background: Chemotherapy cardiotoxicity is an emerging problem and it is very important to prevent cardiac dysfunction caused by anticancer drugs. The aim of this study was to assess the alterations of the cardiac function induced by chemotherapy in a follow-up of 2 years and to evaluate the cardioprotective role of angiotensin-converting enzyme inhibitors (ACEIs) in the prevention of cardiac dysfunction. Methods: A prospective study was carried out using patients with breast cancer (85 women; median age 57W12years) and other inclusion and exclusion criteria. On the basis of treatment, patients were divided into six groups: fluorouracil-epirubicincyclophosphamide, FEC (group A); FEC and tra…

Cardiac function curveAdultmedicine.medical_specialtyCardiotonic Agentsmedicine.medical_treatmentAngiotensin-Converting Enzyme InhibitorsBreast Neoplasms030204 cardiovascular system & hematologyBioinformaticsCardiac dysfunctionAngiotensin-converting enzyme inhibitor; Cardiotoxicity; Chemotherapy; Prevention; Tissue Doppler imaging; Adult; Aged; Aged 80 and over; Angiotensin-Converting Enzyme Inhibitors; Antineoplastic Combined Chemotherapy Protocols; Breast Neoplasms; Cardiotonic Agents; Cardiotoxicity; Early Diagnosis; Echocardiography Doppler; Female; Follow-Up Studies; Humans; Middle Aged; Prospective Studies03 medical and health sciencesTissue Doppler imaging0302 clinical medicinecardiac toxicity anti cancer drugs cardiac dysfunctionInternal medicineAntineoplastic Combined Chemotherapy Protocols80 and overMedicineChemotherapyHumansProspective StudiesAgedAged 80 and overCardiotoxicityChemotherapybusiness.industryPreventionFollow up studiesDopplerGeneral MedicineMiddle AgedCardiotoxicityEchocardiography DopplerClinical trialEarly DiagnosisAngiotensin-converting enzyme inhibitorEchocardiography030220 oncology & carcinogenesiscardiovascular systemCardiologyFemaleCardiology and Cardiovascular MedicinebusinessFollow-Up StudiesJournal of cardiovascular medicine (Hagerstown, Md.)
researchProduct

0131 : Impact of overweight on anthracycline and trastuzumab-induced cardiotoxicity: experimental study in mice

2015

Trastuzumab (TRZ), a humanized monoclonal antibody against Human Epidermal Growth Factor Receptor 2 (HER2) oncogene, is believed to potentiate doxorubicin (DOX) cardiotoxicity, resulting in left ventricular dysfunction. Few data indicate that overweight could influence DOX-induced cardiotoxicity, and no study has already evaluated the impact of moderate overweight on the cardiotoxic effect of DOX alone or in combination with TRZ. Immediately after birth, litters of C57BL/6 mice were either maintained at 10 (normal litter, NL), or reduced to 3 (small litter, SL) in order to induce programming of ~15% overweight through postnatal overfeeding. At 4 months, in order to evaluate the potentiation…

Cardiac function curveCardiotoxicitymedicine.medical_specialtyEjection fractionOncogeneAnthracyclinebusiness.industrymedicine.medical_treatmentIntraperitoneal injectionEndocrinologyTrastuzumabInternal medicinepolycyclic compoundsMedicineDoxorubicinCardiology and Cardiovascular Medicinebusinessmedicine.drugArchives of Cardiovascular Diseases Supplements
researchProduct

Dystrophin-deficiency increases the susceptibility to doxorubicin-induced cardiotoxicity

2007

Background and aim: The clinical use of doxorubicin (DOX) and other anthracyclines is limited by a dosage-dependent cardiotoxicity, which can lead to cardiomyopathy. The role of the individual genetic makeup in this disorder is poorly understood. Alterations in genes encoding cardiac cytoskeleton or sarcolemma proteins may increase the susceptibility to doxorubicin-related cardiotoxicity. Methods: Female dystrophin-deficient mice (MDX) and age-matched wild-type mice underwent chronic treatment with doxorubicin. Cardiac function and tissue damage were assessed by echocardiography and histopathology, respectively. Gene expression changes were investigated using microarrays. Results: DOX treat…

Cardiac function curveProgrammed cell deathPathologymedicine.medical_specialtyHeart DiseasesCytoskeleton organizationCardiomyopathyGene Expression030204 cardiovascular system & hematologyDystrophinMice03 medical and health sciences0302 clinical medicineRisk FactorsmedicineAnimalsDoxorubicinUltrasonography030304 developmental biology0303 health sciencesCardiotoxicityAntibiotics AntineoplasticSarcolemmabiologybusiness.industryGenetic VariationMicroarray Analysismedicine.disease3. Good healthDoxorubicinDisease Progressionbiology.proteinCancer researchFemaleDisease SusceptibilityCardiology and Cardiovascular MedicineDystrophinbusinessmedicine.drugEuropean Journal of Heart Failure
researchProduct

Doxorubicin induces wide-spread transcriptional changes in the myocardium of hearts distinguishing between mice with preserved and impaired cardiac f…

2021

Abstract Aims Doxorubicin (DOX) is an important drug for the treatment of various tumor entities. However, the occurrence of heart failure limits its application. This study investigated differential gene expression profiles in the left and right ventricles of DOX treated mice with either preserved or impaired myocardial function. We provide new mechanistic insights into the pathophysiology of DOX-induced heart failure and have discovered pathways that counteract DOX-induced cardiotoxicity. Main methods We used in total 48 male mice and applied a chronic low dose DOX administration (5 mg/kg per injection, in total 20 mg/kg over 4 weeks) to induce heart failure. Echocardiographic parameters …

Cardiac function curveTranscription GeneticPharmacologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyElectrocardiographypolycyclic compoundsmedicineAnimalsCluster AnalysisDoxorubicinGeneral Pharmacology Toxicology and Pharmaceuticschemistry.chemical_classificationReactive oxygen speciesCardiotoxicitybusiness.industryGene Expression ProfilingMyocardiumGeneral Medicinemedicine.diseasePathophysiologyMice Inbred C57BLGene expression profilingOxidative StresschemistryDoxorubicinHeart failureHeart Function TestsbusinessOxidative stressmedicine.drugLife Sciences
researchProduct

Iron overload does not potentiate doxorubicin induced cardiotoxicity in vivo in mice and in vitro in cardiomyocytes cell cultures

2013

Background: Doxorubicin (DOX), an anticancer anthracycline, is known to induce serious cardiotoxicity, which is believed to be mediated by oxidative stress and complex interactions with iron. However, the relations between iron metabolism and DOX-induced cardiotoxicity remain a matter of controversy. Methods: Firstly, we used an in vivo murine model of iron overloading (IO) where male C57BL/6 mice received during 3 weeks (D0-D20) a daily dextran-iron injection (15 mg/kg/day.) and then (D21) a single dose of 6 mg/kg DOX. We evaluated cardiac function with echocardiography, myocardial gene's expression, nitro-oxidative stress levels and iron status. Secondly, the anti-proliferative activity o…

Cardiac function curvemedicine.medical_specialtyCardiotoxicityAnthracyclinebusiness.industrymedicine.disease_causeEndocrinologyAtrial natriuretic peptideIn vivoInternal medicinepolycyclic compoundsmedicineDoxorubicinViability assayCardiology and Cardiovascular MedicinebusinessOxidative stressmedicine.drugEuropean Heart Journal
researchProduct

Cardiotoxicity of mitoxantrone treatment in a german cohort of 639 multiple sclerosis patients

2014

Background and PurposezzThe aim of this study was to elucidate the role of therapy-related cardiotoxicity in multiple sclerosis (MS) patients treated with mitoxantrone and to identify potential predictors for individual risk assessment. MethodszzWithin a multicenter retrospective cohort design, cardiac side effects attributed to mitoxantrone were analyzed in 639 MS patients at 2 MS centers in Germany. Demographic, disease, treatment, and follow-up data were collected from hospital records. Patients regularly received cardiac monitoring during the treatment phase. ResultszzNone of the patients developed symptomatic congestive heart failure. However, the frequency of patients experiencing car…

Cardiac function curvemedicine.medical_specialtyCardiotoxicityMitoxantronedose dependencybusiness.industryCumulative doseMultiple sclerosiscardiotoxicityRetrospective cohort studymultiple sclerosismedicine.diseasemitoxantroneNeurologyInternal medicineCohortmedicineOriginal ArticleNeurology (clinical)Risk factorbusinessIntensive care medicineFunction and Dysfunction of the Nervous Systemmedicine.drug
researchProduct