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dc.contributor.authorHortu, Ismet
dc.contributor.authorOzceltik, Gokay
dc.contributor.authorErgenoglu, Ahmet Mete
dc.contributor.authorYigitturk, Gurkan
dc.contributor.authorAtasoy, Ozum
dc.contributor.authorErbas, Oytun
dc.date.accessioned2020-12-02T18:01:33Z
dc.date.available2020-12-02T18:01:33Z
dc.date.issued2020
dc.identifier.issn0932-0067
dc.identifier.issn1432-0711
dc.identifier.urihttps://doi.org/10.1007/s00404-020-05534-1
dc.identifier.urihttp://hdl.handle.net/11446/3653
dc.descriptionOzceltik, Gokay/0000-0003-1413-685Xen_US
dc.descriptionWOS: 000524622800003en_US
dc.descriptionPubMed: 32266527en_US
dc.description.abstractPurpose Although cancer predominantly affects people at older ages, a substantial number of patients, like breast cancer patients, are diagnosed before they have completed their families or even before giving birth. Furthermore, cytotoxic chemotherapy may be required in addition to treat cancer survivors. the present study was conducted to investigate the protective effect of oxytocin (OT) on methotrexate (MTX)-induced ovarian toxicity in rats. Methods Eighteen adult female Sprague-Dawley rats were used in the study. All rats were divided randomly into three groups. the control group (n = 6) received no treatment. the remaining 12 rats received a single dose of 20 mg/kg of MTX. Half of the rats (n = 6) were treated with 1 mg/kg/day of saline, and the other half (n = 6) were treated with 160 mu g/kg/day of OT for 21 days. Then, blood samples were collected for biochemical analysis, and an ovariectomy was performed for histopathological examination. Results Plasma malondialdehyde (MDA) and transforming growth factor-beta (TGF-beta) levels were significantly lower in the MTX + OT group compared to the MTX + saline group (p = 0.000036 for MDA; p = 0.0044 for TGF-beta). AMH levels were also significantly higher in the MTX + OT group than in the MTX + saline group (p = 0.000036). the ovarian fibrosis percent was also notably lower in the MTX + OT group than in the MTX + saline group (p = 0.000036). Conclusion on the basis of these findings, OT is a promising agent for ameliorating harmful effects of MTX on rat ovaries in an experimental model.en_US
dc.language.isoengen_US
dc.publisherSpringer Heidelbergen_US
dc.identifier.doi10.1007/s00404-020-05534-1en_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectMethotrexateen_US
dc.subjectOvarian damageen_US
dc.subjectOxytocinen_US
dc.subjectCytotoxic chemotherapyen_US
dc.subjectAnti-mullerian hormoneen_US
dc.titleProtective effect of oxytocin on a methotrexate-induced ovarian toxicity modelen_US
dc.typearticleen_US
dc.relation.journalArchives of Gynecology and Obstetricsen_US
dc.departmentDBÜen_US
dc.identifier.issue5en_US
dc.identifier.volume301en_US
dc.identifier.startpage1317en_US
dc.identifier.endpage1324en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.department-temp[Hortu, Ismet; Ozceltik, Gokay; Ergenoglu, Ahmet Mete] Ege Univ, Dept Obstet & Gynecol, Sch Med, Izmir, Turkey; [Hortu, Ismet] Ege Univ, Dept Stem Cell, Inst Hlth Sci, Izmir, Turkey; [Yigitturk, Gurkan] Mugla Sitki Kocman Univ, Dept Histol & Embryol, Sch Med, Mugla, Turkey; [Atasoy, Ozum] Univ Hlth Sci Kartal Lutfi Kirdar Educ & Res Hosp, Dept Radiat Oncol, Istanbul, Turkey; [Erbas, Oytun] Demiroglu Bilim Univ, Dept Physiol, Sch Med, Istanbul, Turkeyen_US


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