Differential Effects of Maternal Stress on Circulating Levels of Corticosterone, Progesterone, and Testosterone in Male and Female Rat Fetuses and Their Mothers*

Abstract

Testosterone, progesterone, and corticosterone titers were measured by RIA in plasma of stressed and control pregnant rats and their male and female fetuses on days 17, 18, 19, and 21 of gestation and on the day of birth. The regimen of stress used (three 45-min periods of restraint under intense illumination daily from days 14-21 of pregnancy) causes failure of masculinization and defeminization of behavioral potentials in male offspring. In fetuses of both sexes, corticosterone titers increased sharply between days 17 and 18 postconception (pc) to a peak that was maintained through day 19 and then declined. This pattern resembled that obtained for testosterone in control male fetuses in which the levels of testosterone also rose sharply between days 17 and 18 pc. Corticosterone titers were elevated in samples obtained during the middle of the stress session from both the mothers (serum) and their male and female fetuses (plasma). Increased corticosterone levels were no longer evident in samples obtained from fetuses 75-165 min after the end of a stress session. Testosterone titers were altered by stress only in male fetuses. Their testosterone levels were elevated on day 17 pc, and the surge on days 18 and 19 pc, characteristic of control males, was absent in samples obtained 75-165 min after termination of stress. Progesterone titers were not affected by stress in either mothers or their fetuses. In both stressed and control groups, progesterone concentrations were identical in male and female fetuses, were higher in mothers than in fetuses, and declined in both fetuses and mothers between days 19 and 21 pc. Thus, a persistent effect of stress was observed only on testosterone and only in males.

Maternal obesity disturbs the postnatal development of gonocytes in the rat without impairment of testis structure at prepubertal age

“…Thus, the numerical values obtained for each animal and the means for each group suggest that MO interferes in neonatal steroidogenesis. Male rats normally experience a surge in plasma testosterone during 18 and 19 dpc (Ward & Weisz 1984) and another peak is observed during the first few hours following birth (Corbier et al 1992). Several reports indicate that stress-induced hormonal changes in pregnant mother and/or male fetuses may affect plasma testosterone surges in late stages of pregnancy or post partum (Ward 1972, Ward & Weisz 1984, Pereira et al 2003.…”

“…Male rats normally experience a surge in plasma testosterone during 18 and 19 dpc (Ward & Weisz 1984) and another peak is observed during the first few hours following birth (Corbier et al 1992). Several reports indicate that stress-induced hormonal changes in pregnant mother and/or male fetuses may affect plasma testosterone surges in late stages of pregnancy or post partum (Ward 1972, Ward & Weisz 1984, Pereira et al 2003. In this study, births were nocturnal and death of animals and plasma collection were always made at 0900 h. Although the analysis of prenatal testosterone levels was not the focus of this study, the lower testosterone levels observed for pups from obese mothers at 0.5 dpp strongly indicate that MO might have affected the testosterone neonatal peak, which usually occurs in the first hours after birth.…”

Estrogen receptor-α mediates estrogen-inducible abnormalities in the developing penis

“…It is also known that dihydrotestosterone, a 5a-reductase reduced testosterone metabolite, is more critical than testosterone in development of those organs which are derived from the urogenital sinus, genital tubercle, and genital swelling in males, including the penis (Anderson & Clark 1990, George & Wilson 1994. Notably, the early differentiation and morphogenesis of male reproductive organs corresponds to the testosterone surge by fetal Leydig cells that occurs at about 12 weeks of gestation in humans (Williams-Ashman & Reddi 1991, George & Wilson 1994, Klonisch et al 2004 and at late gestation and early neonatal period in rodents (Ward & Weisz 1984, El-Gehani et al 1998. Alterations in androgenic activity during the critical period of differentiation, resulting from abnormalities in testosterone, 5a-reductase, or androgen receptor, cause maldevelopment of internal and external male genitalia, including hypospadias and shorter penis (Gray et al 2001, Sultan et al 2001, Kim et al 2002, Foster & Harris 2005.…”

Growth and reproductive development of male piglets are more vulnerable to midgestation maternal stress than that of female piglets12

“…In sheep, maternal undernutrition can reduce development of the testes (Bielli et al, 2002) and lamb yield (Long et al, 2010). Rodent study results suggest maternal GC may suppress fetal androgen synthesis in male progeny (Ward and Weisz, 1984;von Holst, 1998), whereas increases in maternal androgens may alter female progeny .…”