Corticosteroids deeply depress the in vitro steroidogenic capacity of Eurasian perch ovary at the end of the reproductive cycle

Robert Mandiki, S. Milla, Silvia NKOGO ROBLES, P. Kestemont

Résultats de recherche: Contribution à un journal/une revueArticle

Résumé

Corticosteroids play positive or negative role in the reproductive mechanisms of many fish species but the physiological contexts relating to such biphasic actions are not well defined. In the present study we investigated to what extent corticosteroids (cortisol-Co, 11-deoxycorticosterone-DOC) hormones may interfere with the steroidogenic capacity of Eurasian perch ovarian tissues, and we tested whether the negative effects of corticosteroids may be mitigated by potential stimulating endocrine factors, namely insulin-like growth factor-1 (IGF), human chorionic gonadotropin (HCG) or thyroid hormones (Triidothyronine-T3, thyroxine-T4). Ovarian tissues from six maturing fish at late vitellogenesis developmental stage (LVO) or at the start of the final meiotic oocyte maturation (FMO) were incubated during 6 h in Cortland medium containing various endocrine compounds. Both corticosteroids drastically suppressed aromatase activity (AA) and sex-steroid production, namely 17-β estradiol (E2), 17α-20β-dihydroxy-4-pregnen-3-one (DHP) and testosterone (T). HCG significantly prevented the suppression of both AA and sex-steroid production by low and high cortisol doses, but a lesser AA protection was observed in the case of DOC. The protection of DHP and T productions by HCG from the negative effects by the two corticosteroids was higher at FMO than at LVO stage. IGF or thyroid hormone treatments were lesser effective or ineffective in mitigating the suppression of AA or sex-steroid production by cortisol. The results suggest that an increase in cortisol or DOC such as after mild or high stress intensity may inhibit drastically the ovarian steroidogenic capacity whatever the final oocyte maturation stage in percid fish by hampering AA and sex-steroid production. That inhibition may be partly mitigated by gonadotropins but not IGF nor thyroid hormones, especially at final meiotic oocyte maturation stage.

langueAnglais
Pages44-54
Nombre de pages11
journalGeneral and Comparative Endocrinology
Volume245
Les DOIs
étatPublié - 1 mai 2017

Empreinte digitale

Perches
Aromatase
Perca fluviatilis
adrenal cortex hormones
Ovary
Adrenal Cortex Hormones
steroids
Oocytes
cortisol
Hydrocortisone
human chorionic gonadotropin
somatomedins
Somatomedins
oocytes
Chorionic Gonadotropin
thyroid hormones
Steroids
Fishes
gender
Thyroid Hormones

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    title = "Corticosteroids deeply depress the in vitro steroidogenic capacity of Eurasian perch ovary at the end of the reproductive cycle",
    abstract = "Corticosteroids play positive or negative role in the reproductive mechanisms of many fish species but the physiological contexts relating to such biphasic actions are not well defined. In the present study we investigated to what extent corticosteroids (cortisol-Co, 11-deoxycorticosterone-DOC) hormones may interfere with the steroidogenic capacity of Eurasian perch ovarian tissues, and we tested whether the negative effects of corticosteroids may be mitigated by potential stimulating endocrine factors, namely insulin-like growth factor-1 (IGF), human chorionic gonadotropin (HCG) or thyroid hormones (Triidothyronine-T3, thyroxine-T4). Ovarian tissues from six maturing fish at late vitellogenesis developmental stage (LVO) or at the start of the final meiotic oocyte maturation (FMO) were incubated during 6 h in Cortland medium containing various endocrine compounds. Both corticosteroids drastically suppressed aromatase activity (AA) and sex-steroid production, namely 17-β estradiol (E2), 17α-20β-dihydroxy-4-pregnen-3-one (DHP) and testosterone (T). HCG significantly prevented the suppression of both AA and sex-steroid production by low and high cortisol doses, but a lesser AA protection was observed in the case of DOC. The protection of DHP and T productions by HCG from the negative effects by the two corticosteroids was higher at FMO than at LVO stage. IGF or thyroid hormone treatments were lesser effective or ineffective in mitigating the suppression of AA or sex-steroid production by cortisol. The results suggest that an increase in cortisol or DOC such as after mild or high stress intensity may inhibit drastically the ovarian steroidogenic capacity whatever the final oocyte maturation stage in percid fish by hampering AA and sex-steroid production. That inhibition may be partly mitigated by gonadotropins but not IGF nor thyroid hormones, especially at final meiotic oocyte maturation stage.",
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    Corticosteroids deeply depress the in vitro steroidogenic capacity of Eurasian perch ovary at the end of the reproductive cycle. / Mandiki, Robert; Milla, S.; NKOGO ROBLES, Silvia; Kestemont, P.

    Dans: General and Comparative Endocrinology, Vol 245, 01.05.2017, p. 44-54.

    Résultats de recherche: Contribution à un journal/une revueArticle

    TY - JOUR

    T1 - Corticosteroids deeply depress the in vitro steroidogenic capacity of Eurasian perch ovary at the end of the reproductive cycle

    AU - Mandiki,Robert

    AU - Milla,S.

    AU - NKOGO ROBLES,Silvia

    AU - Kestemont,P.

    PY - 2017/5/1

    Y1 - 2017/5/1

    N2 - Corticosteroids play positive or negative role in the reproductive mechanisms of many fish species but the physiological contexts relating to such biphasic actions are not well defined. In the present study we investigated to what extent corticosteroids (cortisol-Co, 11-deoxycorticosterone-DOC) hormones may interfere with the steroidogenic capacity of Eurasian perch ovarian tissues, and we tested whether the negative effects of corticosteroids may be mitigated by potential stimulating endocrine factors, namely insulin-like growth factor-1 (IGF), human chorionic gonadotropin (HCG) or thyroid hormones (Triidothyronine-T3, thyroxine-T4). Ovarian tissues from six maturing fish at late vitellogenesis developmental stage (LVO) or at the start of the final meiotic oocyte maturation (FMO) were incubated during 6 h in Cortland medium containing various endocrine compounds. Both corticosteroids drastically suppressed aromatase activity (AA) and sex-steroid production, namely 17-β estradiol (E2), 17α-20β-dihydroxy-4-pregnen-3-one (DHP) and testosterone (T). HCG significantly prevented the suppression of both AA and sex-steroid production by low and high cortisol doses, but a lesser AA protection was observed in the case of DOC. The protection of DHP and T productions by HCG from the negative effects by the two corticosteroids was higher at FMO than at LVO stage. IGF or thyroid hormone treatments were lesser effective or ineffective in mitigating the suppression of AA or sex-steroid production by cortisol. The results suggest that an increase in cortisol or DOC such as after mild or high stress intensity may inhibit drastically the ovarian steroidogenic capacity whatever the final oocyte maturation stage in percid fish by hampering AA and sex-steroid production. That inhibition may be partly mitigated by gonadotropins but not IGF nor thyroid hormones, especially at final meiotic oocyte maturation stage.

    AB - Corticosteroids play positive or negative role in the reproductive mechanisms of many fish species but the physiological contexts relating to such biphasic actions are not well defined. In the present study we investigated to what extent corticosteroids (cortisol-Co, 11-deoxycorticosterone-DOC) hormones may interfere with the steroidogenic capacity of Eurasian perch ovarian tissues, and we tested whether the negative effects of corticosteroids may be mitigated by potential stimulating endocrine factors, namely insulin-like growth factor-1 (IGF), human chorionic gonadotropin (HCG) or thyroid hormones (Triidothyronine-T3, thyroxine-T4). Ovarian tissues from six maturing fish at late vitellogenesis developmental stage (LVO) or at the start of the final meiotic oocyte maturation (FMO) were incubated during 6 h in Cortland medium containing various endocrine compounds. Both corticosteroids drastically suppressed aromatase activity (AA) and sex-steroid production, namely 17-β estradiol (E2), 17α-20β-dihydroxy-4-pregnen-3-one (DHP) and testosterone (T). HCG significantly prevented the suppression of both AA and sex-steroid production by low and high cortisol doses, but a lesser AA protection was observed in the case of DOC. The protection of DHP and T productions by HCG from the negative effects by the two corticosteroids was higher at FMO than at LVO stage. IGF or thyroid hormone treatments were lesser effective or ineffective in mitigating the suppression of AA or sex-steroid production by cortisol. The results suggest that an increase in cortisol or DOC such as after mild or high stress intensity may inhibit drastically the ovarian steroidogenic capacity whatever the final oocyte maturation stage in percid fish by hampering AA and sex-steroid production. That inhibition may be partly mitigated by gonadotropins but not IGF nor thyroid hormones, especially at final meiotic oocyte maturation stage.

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    KW - Eurasian perch

    KW - Gonadotropins

    KW - Ovarian tissues

    KW - Steroidogenesis

    KW - Thyroid hormones

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