Steroid reduction during ovarian stimulation impairs oocyte fertilization, but not folliculogenesis, in rhesus monkeys

Mary Zelinski, David Hess, D. P. Wolf, Richard Stouffer

    Research output: Contribution to journalArticle

    65 Citations (Scopus)

    Abstract

    Objective: To test the hypothesis that steroids locally modulate and may be required for normal follicular function and gametogenesis in primates, the effects of steroid reduction during gonadotropin-stimulated folliculogenesis was studied in rhesus monkeys. Design: Animals received human FSH (hFSH; days 1 to 6) and hFSH + human LH (hLH; day 7) to promote multiple follicular growth, and then received hCG (day 8) for ovulatory maturation. Four animals received trilostane (3β-hydroxysteroid dehydrogenase inhibitor) on days 1 to 8 or no inhibitor (controls; n = 4). Follicles were aspirated 34 hours after hCG. Main Outcome Measures: Follicular growth, serum E2, P, and pregnenolone, oocyte nuclear maturity, and IVF. Results: Trilostane markedly reduced E2 to levels as low as 7% of controls throughout the follicular phase. Pregnenolone was 66 fold greater during trilostane treatment relative to controls. In both groups, P was at baseline during follicular stimulation but was reduced for 72 hours after hCG in trilostane-treated animals. Despite E2 suppression, follicular growth and oocyte nuclear maturity were unaltered by trilostane. Trilostane hindered the fertilizability of metaphase II oocytes (15%) in three of four animals compared with controls (65%). Metaphase I oocytes that required >8 hours to complete meiosis in vitro failed to fertilize in the same three of four receiving trilostane relative to controls (31%). Conclusions: Follicular growth and oocyte meiosis did not require high or increasing E2 levels. Levels of follicular products other than E2 may be of value in determining the progress of ovarian stimulation protocols. However, the acquisition of oocyte competence for fertilization may require steroids.

    Original languageEnglish (US)
    Pages (from-to)1147-1155
    Number of pages9
    JournalFertility and Sterility
    Volume61
    Issue number6
    StatePublished - 1994

    Fingerprint

    Ovulation Induction
    Macaca mulatta
    Fertilization
    Oocytes
    Steroids
    Human Follicle Stimulating Hormone
    Pregnenolone
    Meiosis
    Metaphase
    Growth
    3-Hydroxysteroid Dehydrogenases
    Gametogenesis
    Follicular Phase
    trilostane
    Gonadotropins
    Mental Competency
    Primates
    Outcome Assessment (Health Care)
    Serum

    Keywords

    • Follicular stimulation
    • IVF
    • oocyte maturation
    • rhesus monkeys
    • steroid reduction during folliculogenesis

    ASJC Scopus subject areas

    • Obstetrics and Gynecology

    Cite this

    Steroid reduction during ovarian stimulation impairs oocyte fertilization, but not folliculogenesis, in rhesus monkeys. / Zelinski, Mary; Hess, David; Wolf, D. P.; Stouffer, Richard.

    In: Fertility and Sterility, Vol. 61, No. 6, 1994, p. 1147-1155.

    Research output: Contribution to journalArticle

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    abstract = "Objective: To test the hypothesis that steroids locally modulate and may be required for normal follicular function and gametogenesis in primates, the effects of steroid reduction during gonadotropin-stimulated folliculogenesis was studied in rhesus monkeys. Design: Animals received human FSH (hFSH; days 1 to 6) and hFSH + human LH (hLH; day 7) to promote multiple follicular growth, and then received hCG (day 8) for ovulatory maturation. Four animals received trilostane (3β-hydroxysteroid dehydrogenase inhibitor) on days 1 to 8 or no inhibitor (controls; n = 4). Follicles were aspirated 34 hours after hCG. Main Outcome Measures: Follicular growth, serum E2, P, and pregnenolone, oocyte nuclear maturity, and IVF. Results: Trilostane markedly reduced E2 to levels as low as 7{\%} of controls throughout the follicular phase. Pregnenolone was 66 fold greater during trilostane treatment relative to controls. In both groups, P was at baseline during follicular stimulation but was reduced for 72 hours after hCG in trilostane-treated animals. Despite E2 suppression, follicular growth and oocyte nuclear maturity were unaltered by trilostane. Trilostane hindered the fertilizability of metaphase II oocytes (15{\%}) in three of four animals compared with controls (65{\%}). Metaphase I oocytes that required >8 hours to complete meiosis in vitro failed to fertilize in the same three of four receiving trilostane relative to controls (31{\%}). Conclusions: Follicular growth and oocyte meiosis did not require high or increasing E2 levels. Levels of follicular products other than E2 may be of value in determining the progress of ovarian stimulation protocols. However, the acquisition of oocyte competence for fertilization may require steroids.",
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    N2 - Objective: To test the hypothesis that steroids locally modulate and may be required for normal follicular function and gametogenesis in primates, the effects of steroid reduction during gonadotropin-stimulated folliculogenesis was studied in rhesus monkeys. Design: Animals received human FSH (hFSH; days 1 to 6) and hFSH + human LH (hLH; day 7) to promote multiple follicular growth, and then received hCG (day 8) for ovulatory maturation. Four animals received trilostane (3β-hydroxysteroid dehydrogenase inhibitor) on days 1 to 8 or no inhibitor (controls; n = 4). Follicles were aspirated 34 hours after hCG. Main Outcome Measures: Follicular growth, serum E2, P, and pregnenolone, oocyte nuclear maturity, and IVF. Results: Trilostane markedly reduced E2 to levels as low as 7% of controls throughout the follicular phase. Pregnenolone was 66 fold greater during trilostane treatment relative to controls. In both groups, P was at baseline during follicular stimulation but was reduced for 72 hours after hCG in trilostane-treated animals. Despite E2 suppression, follicular growth and oocyte nuclear maturity were unaltered by trilostane. Trilostane hindered the fertilizability of metaphase II oocytes (15%) in three of four animals compared with controls (65%). Metaphase I oocytes that required >8 hours to complete meiosis in vitro failed to fertilize in the same three of four receiving trilostane relative to controls (31%). Conclusions: Follicular growth and oocyte meiosis did not require high or increasing E2 levels. Levels of follicular products other than E2 may be of value in determining the progress of ovarian stimulation protocols. However, the acquisition of oocyte competence for fertilization may require steroids.

    AB - Objective: To test the hypothesis that steroids locally modulate and may be required for normal follicular function and gametogenesis in primates, the effects of steroid reduction during gonadotropin-stimulated folliculogenesis was studied in rhesus monkeys. Design: Animals received human FSH (hFSH; days 1 to 6) and hFSH + human LH (hLH; day 7) to promote multiple follicular growth, and then received hCG (day 8) for ovulatory maturation. Four animals received trilostane (3β-hydroxysteroid dehydrogenase inhibitor) on days 1 to 8 or no inhibitor (controls; n = 4). Follicles were aspirated 34 hours after hCG. Main Outcome Measures: Follicular growth, serum E2, P, and pregnenolone, oocyte nuclear maturity, and IVF. Results: Trilostane markedly reduced E2 to levels as low as 7% of controls throughout the follicular phase. Pregnenolone was 66 fold greater during trilostane treatment relative to controls. In both groups, P was at baseline during follicular stimulation but was reduced for 72 hours after hCG in trilostane-treated animals. Despite E2 suppression, follicular growth and oocyte nuclear maturity were unaltered by trilostane. Trilostane hindered the fertilizability of metaphase II oocytes (15%) in three of four animals compared with controls (65%). Metaphase I oocytes that required >8 hours to complete meiosis in vitro failed to fertilize in the same three of four receiving trilostane relative to controls (31%). Conclusions: Follicular growth and oocyte meiosis did not require high or increasing E2 levels. Levels of follicular products other than E2 may be of value in determining the progress of ovarian stimulation protocols. However, the acquisition of oocyte competence for fertilization may require steroids.

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