Effects of alcohol on intraovarian nitric oxide synthase and steroidogenic acute regulatory protein in the prepubertal female rhesus monkey

Vinod K. Srivastava, Gregory Dissen, Sergio Ojeda, Jill K. Hiney, Michelle D. Pine, W. Les Dees

    Research output: Contribution to journalArticle

    7 Citations (Scopus)

    Abstract

    Objective: In addition to affecting hypothalamic-pituitary function, alcohol is a gonadal toxin capable of inhibiting ovarian function and suppressing circulating levels of estradiol (E2) in female rats, rhesus monkeys, and adolescent girls. Both nitric oxide (NO) and steroidogenic acute regulatory protein (StAR) are intraovarian substances that influence steroidogenesis in opposite directions. This study was undertaken to determine whether alcohol exposure affects prepubertal ovarian steroidogenesis in female rhesus monkeys by altering nitric oxide synthase (NOS), StAR, or both. Method: At 20 months of age, monkeys received a single intragastric dose of alcohol (2.4 g/kg) or an equal volume of a saline/sucrose solution daily until they were 36 months old. Blood and ovaries were then collected for assessment of serum hormone levels and tissue gene and protein expression. Results: Alcohol caused depressed levels of serum E2 (p <.05) and luteinizing hormone (p <.05) but not follicle-stimulating hormone. Real-time polymerase chain reaction (RT-PCR) assessment of ovarian mRNA encoding the three isoforms (i.e., neuronal [n] NOS, endothelial [e] NOS, and inducible [i] NOS) of NOS revealed that alcohol exposure did not alter gene expression of nNOS but caused increased basal levels of eNOS (p <.05) and iNOS (p <.01) mRNA expression compared with control ovaries. Alcohol also increased expression of eNOS (p <.01) and iNOS (p <.05) proteins. In contrast, ovaries from monkeys exposed to alcohol showed decreased (p <.05) StAR gene expression compared with controls. Conclusions: We showed previously that alcohol exposure during adolescence suppressed E2 and delayed development of regular monthly menstruation patterns in rhesus monkeys. The present results suggest that the combined action of alcohol to elevate ovarian NOS and suppress StAR synthesis contributes to these abnormalities.

    Original languageEnglish (US)
    Pages (from-to)182-191
    Number of pages10
    JournalJournal of Studies on Alcohol and Drugs
    Volume68
    Issue number2
    StatePublished - Mar 2007

    Fingerprint

    Macaca mulatta
    Nitric Oxide Synthase
    alcohol
    Alcohols
    Ovary
    Gene Expression
    Gene expression
    Haplorhini
    steroidogenic acute regulatory protein
    menstruation
    Nitric Oxide Synthase Type I
    Messenger RNA
    Menstruation
    Nitric Oxide Synthase Type III
    Polymerase chain reaction
    Follicle Stimulating Hormone
    Nitric Oxide Synthase Type II
    Regulator Genes
    Luteinizing Hormone
    Serum

    ASJC Scopus subject areas

    • Medicine (miscellaneous)
    • Psychology(all)
    • Psychiatry and Mental health
    • Toxicology
    • Health(social science)

    Cite this

    Effects of alcohol on intraovarian nitric oxide synthase and steroidogenic acute regulatory protein in the prepubertal female rhesus monkey. / Srivastava, Vinod K.; Dissen, Gregory; Ojeda, Sergio; Hiney, Jill K.; Pine, Michelle D.; Les Dees, W.

    In: Journal of Studies on Alcohol and Drugs, Vol. 68, No. 2, 03.2007, p. 182-191.

    Research output: Contribution to journalArticle

    Srivastava, Vinod K. ; Dissen, Gregory ; Ojeda, Sergio ; Hiney, Jill K. ; Pine, Michelle D. ; Les Dees, W. / Effects of alcohol on intraovarian nitric oxide synthase and steroidogenic acute regulatory protein in the prepubertal female rhesus monkey. In: Journal of Studies on Alcohol and Drugs. 2007 ; Vol. 68, No. 2. pp. 182-191.
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    abstract = "Objective: In addition to affecting hypothalamic-pituitary function, alcohol is a gonadal toxin capable of inhibiting ovarian function and suppressing circulating levels of estradiol (E2) in female rats, rhesus monkeys, and adolescent girls. Both nitric oxide (NO) and steroidogenic acute regulatory protein (StAR) are intraovarian substances that influence steroidogenesis in opposite directions. This study was undertaken to determine whether alcohol exposure affects prepubertal ovarian steroidogenesis in female rhesus monkeys by altering nitric oxide synthase (NOS), StAR, or both. Method: At 20 months of age, monkeys received a single intragastric dose of alcohol (2.4 g/kg) or an equal volume of a saline/sucrose solution daily until they were 36 months old. Blood and ovaries were then collected for assessment of serum hormone levels and tissue gene and protein expression. Results: Alcohol caused depressed levels of serum E2 (p <.05) and luteinizing hormone (p <.05) but not follicle-stimulating hormone. Real-time polymerase chain reaction (RT-PCR) assessment of ovarian mRNA encoding the three isoforms (i.e., neuronal [n] NOS, endothelial [e] NOS, and inducible [i] NOS) of NOS revealed that alcohol exposure did not alter gene expression of nNOS but caused increased basal levels of eNOS (p <.05) and iNOS (p <.01) mRNA expression compared with control ovaries. Alcohol also increased expression of eNOS (p <.01) and iNOS (p <.05) proteins. In contrast, ovaries from monkeys exposed to alcohol showed decreased (p <.05) StAR gene expression compared with controls. Conclusions: We showed previously that alcohol exposure during adolescence suppressed E2 and delayed development of regular monthly menstruation patterns in rhesus monkeys. The present results suggest that the combined action of alcohol to elevate ovarian NOS and suppress StAR synthesis contributes to these abnormalities.",
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    T1 - Effects of alcohol on intraovarian nitric oxide synthase and steroidogenic acute regulatory protein in the prepubertal female rhesus monkey

    AU - Srivastava, Vinod K.

    AU - Dissen, Gregory

    AU - Ojeda, Sergio

    AU - Hiney, Jill K.

    AU - Pine, Michelle D.

    AU - Les Dees, W.

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    AB - Objective: In addition to affecting hypothalamic-pituitary function, alcohol is a gonadal toxin capable of inhibiting ovarian function and suppressing circulating levels of estradiol (E2) in female rats, rhesus monkeys, and adolescent girls. Both nitric oxide (NO) and steroidogenic acute regulatory protein (StAR) are intraovarian substances that influence steroidogenesis in opposite directions. This study was undertaken to determine whether alcohol exposure affects prepubertal ovarian steroidogenesis in female rhesus monkeys by altering nitric oxide synthase (NOS), StAR, or both. Method: At 20 months of age, monkeys received a single intragastric dose of alcohol (2.4 g/kg) or an equal volume of a saline/sucrose solution daily until they were 36 months old. Blood and ovaries were then collected for assessment of serum hormone levels and tissue gene and protein expression. Results: Alcohol caused depressed levels of serum E2 (p <.05) and luteinizing hormone (p <.05) but not follicle-stimulating hormone. Real-time polymerase chain reaction (RT-PCR) assessment of ovarian mRNA encoding the three isoforms (i.e., neuronal [n] NOS, endothelial [e] NOS, and inducible [i] NOS) of NOS revealed that alcohol exposure did not alter gene expression of nNOS but caused increased basal levels of eNOS (p <.05) and iNOS (p <.01) mRNA expression compared with control ovaries. Alcohol also increased expression of eNOS (p <.01) and iNOS (p <.05) proteins. In contrast, ovaries from monkeys exposed to alcohol showed decreased (p <.05) StAR gene expression compared with controls. Conclusions: We showed previously that alcohol exposure during adolescence suppressed E2 and delayed development of regular monthly menstruation patterns in rhesus monkeys. The present results suggest that the combined action of alcohol to elevate ovarian NOS and suppress StAR synthesis contributes to these abnormalities.

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