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Prenatal stress effects over two generations in rats.

I Pollard

    The Journal of Endocrinology
    |May 1, 1986
    PubMed
    Summary

    Maternal stress during pregnancy caused persistent growth deficits in second-generation rats. While their stress response was intact, males showed altered hormone levels and testicular enzyme activity, suggesting transgenerational effects.

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    Area of Science:

    • Endocrinology
    • Developmental Biology
    • Reproductive Science

    Background:

    • Prenatal stress exposure can induce long-term physiological and behavioral changes in offspring.
    • Transgenerational epigenetic inheritance is a mechanism by which parental experiences may influence subsequent generations.

    Purpose of the Study:

    • To investigate the persistent effects of maternal prenatal stress on growth, stress response, reproductive hormones, and testicular enzyme activity in second-generation rats.
    • To assess potential transgenerational impacts of stress across generations.

    Main Methods:

    • Rats were exposed to stress during pregnancy, and their offspring (F2 generation) were monitored for growth and subjected to acute stress.
    • Plasma progesterone and testicular 3 beta-hydroxysteroid dehydrogenase activity were measured in adult male offspring.
    • Fertility of female offspring (F2 generation) was assessed by examining the third-generation (F3) litters.

    Main Results:

    • Second-generation rats exhibited slower growth and were permanently smaller than controls.
    • Adult offspring showed an intact acute stress response.
    • Male offspring from stressed mothers had significantly higher plasma progesterone and lower testicular 3 beta-hydroxysteroid dehydrogenase activity.
    • Female offspring fertility was unaffected, with normal third-generation litter sizes.

    Conclusions:

    • Prenatal stress can lead to lasting growth impairments and altered reproductive physiology in subsequent generations.
    • Specific molecular changes in male offspring suggest potential disruptions in reproductive function.
    • Altered genetic programming or uterine environment may mediate these transgenerational effects.

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