Literature DB >> 21550044

Is anti-Müllerian hormone a marker of acute cyclophosphamide-induced ovarian follicular destruction in mice pretreated with cetrorelix?

Hyacinth N Browne1, Kimberly S Moon, Sunni L Mumford, Enrique F Schisterman, Alan H Decherney, James H Segars, Alicia Y Armstrong.   

Abstract

OBJECTIVE: To define whether anti-Müllerian hormone (AMH) may be a marker of acute cyclophosphamide (CTX)-induced germ cell destruction in mice pretreated with the GnRH antagonist, cetrorelix.
DESIGN: Controlled, experimental study.
SETTING: Research laboratory in a federal research facility. ANIMAL(S): Balb/c female mice (6 weeks old). INTERVENTION(S): Mice were treated with GnRH antagonist (cetrorelix) or saline for 15 days followed by 75 mg/kg or 100 mg/kg of CTX or saline control on day 9. MAIN OUTCOME MEASURE(S): Number of primordial follicles (PMF), DNA damage, AMH protein expression, and AMH serum levels. RESULT(S): Ovaries in mice pretreated with cetrorelix had significantly more PMFs and reduced DNA damage compared with those exposed to CTX alone. Immunohistochemical staining for AMH expression and serum AMH levels did not differ significantly between treatment groups. CONCLUSION(S): Cetrorelix protected PMFs and reduced DNA damage in follicles of mice treated with CTX, but AMH levels in tissue and serum did not correlate with germ cell destruction. Further research is needed to determine the mechanism responsible for the protective effects on PMF counts observed with cetrorelix. Published by Elsevier Inc.

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Year:  2011        PMID: 21550044      PMCID: PMC3129384          DOI: 10.1016/j.fertnstert.2011.04.008

Source DB:  PubMed          Journal:  Fertil Steril        ISSN: 0015-0282            Impact factor:   7.329


  34 in total

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5.  Subclinical depletion of primordial follicular reserve in mice treated with cyclophosphamide: clinical importance and proposed accurate investigative tool.

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6.  Folliculogenesis Is Not Fully Inhibited during GnRH Analogues Treatment in Mice Challenging Their Efficiency to Preserve the Ovarian Reserve during Chemotherapy in This Model.

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