Plasma Testosterone and Progesterone Titers of Pregnant Rats, Their Male and Female Fetuses, and Neonatal Offspring*

Abstract

Testosterone and progesterone titers were determined by RIA in the plasma of pregnant rats and their male and female fetuses from day 17 of gestation through the day of birth and in male and female neonates on days 3 and 5 post partum. Males had significantly higher mean testosterone levels than females from day 18 of gestation through day 5 post partum. Sex differences in plasma testosterone concentrations were greatest in the fetuses on days 18 and 19 of gestation when testosterone levels peaked in the males. Instances in which female fetuses had testosterone titers equal to or greater than their male littermates were found on every day of gestation except day 18. Mean testosterone concentrations in plasma of female fetuses were high throughout gestation (greater than 1000 pcg/ml). Testosterone concentrations decreased in both sexes after birth. Differences between the sexes remained significant, and although there was an overlap in the values for males and females, testosterone concentrations in females exceeded those of their male littermates in only one out of nine pairs of samples on day 5 and in none of seven pairs on day 3 post partum. There were no significant differences in progesterone levels in plasma of males and females, either pre- or postnatally. Progesterone titers changed as a function of days post conception in both the fetuses and their mothers. In the fetuses, progesterone levels declined progressively from day 18 post conception through the day of birth, while in the mother they rose from days 18 to 19 then declined between days 20 and 21 of pregnancy. Fetuses had lower progesterone titers than their mothers. From these data, we conclude that day 18 and possibly day 19 post conception represent a critical period during which the central nervous system of the male is primed by high levels of testosterone. Thereafter, the process of masculinization is completed by exposure to testosterone levels that are relatively low and need not be consistently higher than those of female littermates.

Prenatal androgen exposure causes hypertension and gut microbiota dysbiosis

“…23 , 24 During this period, testosterone peaks between days 17–19. 25 , 26 Excess prenatal androgens (PNA) during this period induce a hypertensive phenotype in adulthood that is characterized by impaired blood flow in the vascular endothelium 12 , increased blood volume 27 , and increased blood pressure in adult females and males. 28 , 29 However, the mechanism by which androgens induce this hypertension is not clear.…”

17β-Estradiol protects the neonatal brain from hypoxia–ischemia

“…By the end of the first postnatal week in rats (when H/I was administered), estradiol levels are naturally waning (Dohler and Wuttke, 1974;Weisz and Ward, 1980). Similarly, following birth, estradiol levels in humans are dropping (Forest, 1979;Corbier et al, 1992).…”

“…testosterone, estradiol, and progesterone) are elevated, comparable to levels in adulthood (Warne et al, 1977;Forest, 1979;Weisz and Ward, 1980;Corbier et al, 1992;Knickmeyer and Baron-Cohen, 2006). Levels of testosterone and estradiol are elevated from embryonic day 17 though embryonic day 21 in rats, with another surge in hormone levels occurring immediately after birth.…”

“…Levels of testosterone and estradiol are elevated from embryonic day 17 though embryonic day 21 in rats, with another surge in hormone levels occurring immediately after birth. Elevated levels persist through the first postnatal week of life in rats (Dohler and Wuttke, 1974;Forest, 1979;Weisz and Ward, 1980;Corbier et al, 1992). In humans, testosterone biosynthesis begins around gestational week 9, with elevated levels of both testosterone and estradiol (due to aromatization from testosterone) persisting through gestational week 24 (Warne et al, 1977;Knickmeyer and Baron-Cohen, 2006).…”

“…The developmental production of steroid hormones (i.e. testosterone, progesterone and estradiol), comes from four distinct sources: 1) originating from the fetus, produced by the gonads or adrenal glands (Gerall et al, 1991), 2) originating from the mother, produced by her gonads and the placenta (Weisz and Ward, 1980), 3) locally converted from a biochemical precursor via the activity of an enzyme such as neuronal aromatase within rat pups (George and Ojeda, 1982), and 4) de novo synthesis in rat pups (Amateau et al, 2004).…”