Partial Inhibition of Estrogen-Induced Mammary Carcinogenesis in Rats by Tamoxifen Balance between Oxidant Stress and Estrogen Responsiveness 英文参考文献.docVIP

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Partial Inhibition of Estrogen-Induced Mammary Carcinogenesis in Rats by Tamoxifen Balance between Oxidant Stress and Estrogen Responsiveness 英文参考文献.doc

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Partial Inhibition of Estrogen-Induced Mammary Carcinogenesis in Rats by Tamoxifen Balance between Oxidant Stress and Estrogen Responsiveness 英文参考文献

PartialInhibitionofEstrogen-InducedMammary CarcinogenesisinRatsbyTamoxifen:Balancebetween OxidantStressandEstrogenResponsiveness BhupendraSingh,NimeeK.Bhat,HariK.Bhat* DivisionofPharmacologyandToxicology,SchoolofPharmacy,UniversityofMissouri-KansasCity,KansasCity,Missouri,UnitedStatesofAmerica Abstract Epidemiological and experimental evidences strongly support the role of estrogens in breast tumor development. Both estrogen receptor (ER)-dependent and ER-independent mechanisms are implicated in estrogen-induced breast carcinogenesis. Tamoxifen, a selective estrogen receptor modulator is widely used as chemoprotectant in human breast cancer.ItbindstoERsandinterfereswithnormalbindingofestrogentoERs.Inthepresentstudy,weexaminedtheeffectof long-termtamoxifentreatmentinthepreventionofestrogen-inducedbreastcancer.FemaleACIratsweretreatedwith17b- estradiol (E2), tamoxifen or with a combination of E2 and tamoxifen for eight months. Tissue levels of oxidative stress markers8-iso-ProstaneF2a(8-isoPGF2a),superoxidedismutase(SOD),glutathioneperoxidase(GPx),catalase,andoxidative DNA damage marker 8-hydroxydeoxyguanosine (8-OHdG) were quantified in the mammary tissues of all the treatment groupsandcomparedwithage-matchedcontrols.LevelsoftamoxifenmetabolizingenzymescytochromeP450saswellas estrogenresponsivegeneswerealsoquantified.Atnecropsy,breasttumorsweredetectedin44%ofratsco-treatedwith tamoxifen+E2.NotumorsweredetectedintheshamortamoxifenonlytreatmentgroupswhereasintheE2onlytreatment group,thetumorincidencewas82%.Co-treatmentwithtamoxifendecreasedGPxandcatalaselevels;didnotcompletely inhibit E2-mediated oxidative DNA damage and estrogen-responsive genes monoamine oxygenase B1 (MaoB1) and cell death inducing DFF45 like effector C (Cidec) but differentially affected the levels of tamoxifen metabolizing enzymes. In summary,ourstudiessuggestthatalthoughtamoxifentreatmentinhibitsestrogen-inducedbreasttumordevelopmentand increasesthelatencyoftumordevelopment,itdoesnotcomplete