Search results for "mammary gland"

showing 10 items of 81 documents

Induction of mitochondrial xanthine oxidase activity during apoptosis in the rat mammary gland

2006

Oxidative stress is an important signal for apoptosis to start. So far the mitochondrial respiratory chain has been considered as the major, if not the only, cause of such stress. Here we report that this is not the case. Xanthine oxidase, a O2(-) and H2O2 generating enzyme which is important in causing significant oxidative stress in the cytosol, is also present in the mitochondrial fraction of rat mammary gland. After weaning, during the involution of the mammary gland, massive apoptosis occurs. Mitochondrial xanthine oxidase activity increases and high mitochondrial H2O2 production takes place. Inhibition of xanthine oxidase activity by allopurinol, a specific inhibitor of xanthine oxida…

Xanthine OxidaseAllopurinolRespiratory chainAllopurinolApoptosisWeaningMitochondrionmedicine.disease_causeMitochondrial Proteinschemistry.chemical_compoundMammary Glands AnimalmedicineAnimalsInvolution (medicine)Enzyme InhibitorsXanthine oxidaseChemistryHydrogen PeroxideMitochondriaRatsCell biologyOxidative StressMitochondrial respiratory chainBiochemistryApoptosisOxidative stressmedicine.drugFrontiers in Bioscience
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Dietary exposure in utero and during lactation to a mixture of genistein and an anti-androgen fungicide in a rat mammary carcinogenesis model

2015

Endocrine disruptors may play substantial roles in the high incidence of breast cancer. We previously described how early exposure to the mixture of phytoestrogen genistein (G) and the anti-androgen vinclozolin (V) affects peripubertal mammary development. This study evaluates the carcinogenic potential of exposure to V alone or associated with G from conception until weaning in Wistar rats. Dams were exposed to V, G or GV during pregnancy/lactation. At PND50 offspring were treated with DMBA[7,12-dimethylbenz(a)anthracene]. V or GV maternal exposure decreased number of DMBA-induced mammary tumors in the offspring, without significant modifications in tumor incidence, multiplicity and latenc…

[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionGenisteinDMBAEndocrine DisruptorsToxicologymedicine.disease_causechemistry.chemical_compound0302 clinical medicinePregnancyRisk FactorsLactationVinclozolinOxazoles0303 health sciencesAge Factorsendocrine disruptionGenisteinTumor Burden3. Good health[ SDV.BDLR ] Life Sciences [q-bio]/Reproductive Biologymedicine.anatomical_structuregestational and lactational exposureReceptors EstrogenMaternal ExposureIn utero030220 oncology & carcinogenesisphytoestrogenFemaleReceptors ProgesteroneCarcinoma in Situmedicine.medical_specialtyendocrine systemanti-androgenOffspring910-Dimethyl-12-benzanthraceneBreast NeoplasmsGestational AgeBiologyRisk Assessment03 medical and health sciencesMammary Glands AnimalPrenatal Educationmammary gland carcinogenesisInternal medicinemedicineAnimalsEndocrine systemRats WistarCell Proliferation030304 developmental biologyAndrogen AntagonistsEpithelial Cells[SDV.BDLR]Life Sciences [q-bio]/Reproductive BiologyDietFungicides IndustrialDisease Models AnimalEndocrinologychemistryCarcinogenesis[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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Abnormal peripubertal development of the rat mammary gland following exposure in utero and during lactation to a mixture of genistein and the food co…

2011

The impact of early exposure to endocrine disruptor mixtures on mammary gland development is poorly known. Here, we identify the effects of a conception to weaning exposure of rats to the phytoestrogen genistein (G) and/or the antiandrogen vinclozolin (V) at 1 mg/kg-d, alone or in association. Using several approaches, we found that G- and GV-exposed rats displayed significantly greater epithelial branching and proliferation, wider terminal end buds than controls at PND35, as well as ductal hyperplasia and periductal fibrosis. Focal branching defects were present in V-exposed rats. An increased ER and AR expression was observed in G- and CV- as compared to V-exposed rats at PND35. Surprisin…

[SDV.BA] Life Sciences [q-bio]/Animal biology[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionreceptorGenisteinmammary gland developmentsprague-dawley ratsToxicologyAntiandrogen[ SDV.BA ] Life Sciences [q-bio]/Animal biologychemistry.chemical_compound0302 clinical medicineLactationSexual MaturationVinclozolinReceptorOxazolesfemale mice0303 health sciences[SDV.BA]Life Sciences [q-bio]/Animal biologyendocrine disruptiondifferentiationGenisteinDrug Combinationsmedicine.anatomical_structuregestational and lactational exposureEndocrine disruptorMaternal ExposureIn utero030220 oncology & carcinogenesisVaginaphytoestrogenFemalemedicine.medical_specialtyanti-androgenbreast-cancer riskmedicine.drug_classgrowthFood ContaminationPhytoestrogensandrogenBiologytransgenic mice03 medical and health sciencesMammary Glands AnimalInternal medicinemedicineAnimalsLactationRats Wistar030304 developmental biologyHyperplasiaBody WeightAndrogen AntagonistsAndrogenRats[SDV.AEN] Life Sciences [q-bio]/Food and Nutritionbisphenol-a alterstumorigenesisEndocrinologychemistrycells[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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Bisphenol A, genistein and vinclozolin: three endocrine disruptors which differentially affect the mammary gland in rats : critical window of exposure

2012

Bisphenol A, genistein and vinclozolin: three endocrine disruptors which differentially affect the mammary gland in rats : critical window of exposure. Colloque PNR-PE

[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismendocrine disruptorperturbateur endocrinienendocrine systemmammary glandurogenital systembisphenol avinclozoline[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutrition[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismgenistein[SDV.AEN] Life Sciences [q-bio]/Food and Nutritiongenistéineglande mammairerat[SDV.AEN]Life Sciences [q-bio]/Food and Nutritionhormones hormone substitutes and hormone antagonists
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Abnormal peripubertal development of the rat mammary gland following exposure in utero and during lactation to a mixture of genistein and the food co…

2012

The impact of early exposure to endocrine disruptor mixtures on mammary gland development is poorly known. Here, we identify the effects of a conception to weaning exposure of rats to the phytoestrogen genistein (G) and/or the antiandrogen vinclozolin (V) at 1 mg/kg-d, alone or in association. Using several approaches, we found that G- and GV-exposed rats displayed significantly greater epithelial branching and proliferation, wider terminal end buds than controls at PND35, as well as ductal hyperplasia and periductal fibrosis. Focal branching defects were present in V-exposed rats. An increased ER and AR expression was observed in G- and CV- as compared to V-exposed rats at PND35. Surprisin…

anti-androgenbreast-cancer risk[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutritionreceptorgrowthsprague-dawley ratsandrogendifferentiationendocrine disruptionmammary gland developmenttransgenic mice[SDV.AEN] Life Sciences [q-bio]/Food and Nutritionbisphenol-a alterstumorigenesisgestational and lactational exposurecellsphytoestrogenfemale mice[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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Cytotoxicity of the Urokinase-Plasminogen Activator Inhibitor Carbamimidothioic Acid (4-Boronophenyl) Methyl Ester Hydrobromide (BC-11) on Triple-Neg…

2015

BC-11 is an easily synthesized simple thiouronium-substituted phenylboronic acid, which has been shown to be cytotoxic on triple negative MDA-MB231 breast cancer cells by inducing a perturbation of cell cycle when administered at a concentration equal to its ED50 at 72 h (117 μM). Exposure of cells to BC-11, either pre-absorbed with a soluble preparation of the N-terminal fragment of urokinase-plasminogen activator (uPa), or in co-treatment with two different EGFR inhibitors, indicated that: (i) BC-11 acts via binding to the N-terminus of the enzyme where uPa- and EGF receptor-recognizing sites are present, thereby abrogating the growth-sustaining effect resulting from receptor binding

boronic acidPharmaceutical ScienceGene ExpressionApoptosisAnalytical ChemistryDrug DiscoveryCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaCytotoxicityEGFR inhibitorschemistry.chemical_classificationCell CycleDrug SynergismCell cycleBoronic AcidsMitochondriaErbB ReceptorsBiochemistryChemistry (miscellaneous)Molecular MedicinecytotoxicityFemaleQD0241Antineoplastic AgentsArticlelcsh:QD241-441plasminogen activator inhibitorbreast cancerlcsh:Organic chemistryCell Line TumorHumansPhysical and Theoretical ChemistryMammary Glands HumanCell ProliferationQD0415Reactive oxygen speciesHydrobromideOrganic ChemistryEpithelial CellsBC-11Molecular biologyUrokinase-Type Plasminogen ActivatorPlasminogen InactivatorsEnzymechemistryApoptosisQuinazolinesMDA-MB231 cellsReactive Oxygen Speciesboronic acid; BC-11; plasminogen activator inhibitor; breast cancer; cytotoxicity; MDA-MB231 cellsMolecules
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Subcellular distribution of calpain-1 and calpain-2 as a key event for calpain-mediated functions in physiological and neoplastic mammary models

2019

Calpains are a family of calcium-dependent proteases, which modulate their substrates rather than degrade them in such a way that modifies them. Calpains deregulations have been determined as an aggravating factor of different diseases, including cancer. Nevertheless, there are no clear records about the particular contribution of each calpain isoform in physiological processes and how these isoforms are deregulated in pathological conditions. In vivo, each calpain isoform recognizes specific proteins as substrates, and it has been suggested that calpains subcellular localization might determine their substrate recognition, and consequently their functions. In the present study we have expl…

breast cancer:CIENCIAS DE LA VIDA::Biología celular [UNESCO]calpain-2UNESCO::CIENCIAS MÉDICASUNESCO::CIENCIAS TECNOLÓGICAS::Tecnología bioquímicacalpain subcellular localizationUNESCO::CIENCIAS DE LA VIDA::Biología celularcalpain-1mammary gland involution:CIENCIAS MÉDICAS [UNESCO]:CIENCIAS TECNOLÓGICAS::Tecnología bioquímica [UNESCO]
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Regulation of the Urea Cycle during Lactation

1990

We have recently shown that the uptake of amino acids by rat lactating mammary gland is 15 mmoles/day (1). This effect is achieved by an increase in food intake during lactation and probably by changes in amino acid metabolism in other tissues. Rat liver removes 75% of the total amino acids derived from a protein meal (2); therefore plays a key role in the regulation of plasma amino acid concentration.

chemistry.chemical_classificationMealMammary glandHigh-protein dietmedicine.disease_causeAmino acidmedicine.anatomical_structureBiochemistrychemistryLactationRat liverUrea cyclemedicineAmino acid metabolism
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Phenotypic and genetic analysis of udder health using SCC in Valle del Belice dairy sheep

2005

Intramammary infections (IMI) are a complex of inflammatory diseases which are defined as an inflammation of the mammary gland resulting from the introduction and multiplication of pathogenic micro-organisms.

intramammary infectionsomatic cell countMammary glandInflammationBiologydairy sheepMilk productionGenetic analysisPhenotypeIntramammary infectionNORWEGIAN CATTLEMILKmedicine.anatomical_structureImmunologymedicineAnimal Science and Zoologyintramammary infection somatic cell count dairy sheep milk productionlcsh:Animal culturemilk productionmedicine.symptomUdderCLINICAL MASTITISSomatic cell countlcsh:SF1-1100Italian Journal of Animal Science
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The L-glutamate transporters GLAST (EAAT1) and GLT-1 (EAAT2): expression and regulation in rat lactating mammary gland.

1999

The Na(+)-dependent L-glutamate transporters GLAST (EAAT1) and GLT-1 (EAAT2), were expressed in rat lactating mammary gland, but EAAC1 (EAAT3) was not. GLT-1 expression in rat lactating mammary gland was constant in all the physiological situations studied; however, the GLAST expression is under tight regulation. Fasting for 24 h decreased the GLAST expression which returned to control values after refeeding. Weaning for 24 h produced a decrease in GLAST expression through a mechanism independent of prolactin deficiency. Resuckling for 6 h returned the expression of this transporter to control values. There is a correlation between the levels of GLAST (mRNA and protein) and the in vivo upta…

medicine.medical_specialtyAmino Acid Transport System X-AGMammary glandBlotting WesternMammary Glands AnimalIn vivoInternal medicineLactationmedicineWeaningAnimalsLactationTissue DistributionRats WistarMolecular BiologyMessenger RNAChemistryReverse Transcriptase Polymerase Chain ReactionTransporterProlactin deficiencyCell BiologyBlotting NorthernRatsBlotmedicine.anatomical_structureEndocrinologyATP-Binding Cassette TransportersFemaleMolecular membrane biology
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