Concentrations of testosterone and androsterone in peripheral and umbilical venous plasma of fetal rats

Vreeburg, J. T. M.; Groeneveld, J. O.; Post, PR; Ooms, M. P.

doi:10.1530/jrf.0.0680171

Cited by 20 publications

(10 citation statements)

References 17 publications

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“…During the critical period of development that extends from day 18 of pregnancy until 8-10 days of life, the hypothalamic structures believed to be involved in the control of normal cyclic hormone secretion are undergoing neuronal maturation. Disruption or modification of hypothalamic maturation has a permanent effect that results in a malelike or acyclic pattern of hormone release and infertility (65)(66)(67)(68)(69). Further investigations are needed to show whether the slight delay in the differentiation of the ovary during fetal life observed in our experiments leads to marked differences in reproductive abilities, such as delay of puberty, lengthening of the estrous cycle, and accelerating the decline in reproductive performance.…”

Section: Discussionmentioning

confidence: 77%

The masculinization of the fetus during pregnancy due to inhalation of diesel exhaust.

Watanabe¹,

Kurita²

2001

Environ Health Perspect

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This study was conducted to determine the impact of diesel exhaust inhalation on the fetus. Seventy-two pregnant rats and 18 nonpregnant rats were divided into three groups: a group exposed to total diesel engine exhaust containing 5.63 mg/m(3) particulate matter, 4.10 ppm nitrogen dioxide, and 8.10 ppm nitrogen oxide; a group exposed to filtered exhaust without particulate matter; and a group exposed to clean air. The exposure period was from day 7 until day 20 of pregnancy. In addition, 15 pregnant rats were treated with aromatase inhibitors or testosterone to clarify the process by which diesel exhaust exerts its toxicity. The anogenital distance was significantly longer in male and female fetuses from both exhaust-exposed groups than in those of the control. Differentiation of the testis, ovary, and thymus was delayed and disturbed. Maternal testosterone and progesterone levels, which increased due to pregnancy whether or not the rats were exposed, were significantly higher and lower, respectively, in the pregnant rats exposed to total exhaust and filtered exhaust. The serum adrenocorticotropic hormone (ACTH) level and urinary excretion of 17-hydroxycorticosteroids (OHCS) did not differ among the pregnant groups. These results indicate that elevated testosterone did not result from elevated maternal adrenal function. The feto-placental-ovarian unit and inhibition of aromatase activity and synthesis caused by diesel exhaust inhalation might have played an essential role in the accumulation of testosterone. Since both exhaust-exposed groups showed almost the same reactions toward the inhalation, the gaseous phase must have included the relevant toxicants.

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Section: Discussionmentioning

confidence: 77%

The masculinization of the fetus during pregnancy due to inhalation of diesel exhaust.

Watanabe¹,

Kurita²

2001

Environ Health Perspect

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“…Further research needs to investigate the extent to which fetuses are affected by endogenous androgens in the maternal circulation, and to identify other factors that might affect the testosterone level of the litter as a whole, In addition, as caudal males accounted for only a small portion of the variance in testosterone, other potential sources of androgens which might affect individual fetuses within the uterus need to be investigated. For example, testosterone production by the placenta during the second half of pregnancy has been demonstrated (10), and several reports have identified the placenta as a major source of androgen in the female fetus (24,33).…”

Section: Discussionmentioning

confidence: 99%

Plasma testosterone in fetal rats and their mothers on day 19 of gestation

Houtsmuller

Jong

Rowland

et al. 1995

Physiology & Behavior

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“…Because prenatal administration of androgens masculinizes females and AR expression is comparable in males and females, it is unclear why females are not more masculinized (George and Wilson 1994). The source(s) of these androgens in female rats is not known, as there is no evidence that developing ovaries could be responsible for androgen production (Vreeburg et al 1983). Several different extra-ovarian sources for the androgens in females have been proposed, including placenta (Baum et al 1991;Vreeburg et al 1983), fetal adrenals (Stahl et al 1991), maternal circulation, or contribution by developing male fetuses (Clark et al 1993;Drickamer et al 1997;Vandenbergh and Huggett 1995;vom Saal et al 1999).…”

Section: Natural Variation In Androgen Concentrations During Developmentmentioning

confidence: 99%

Androgens and environmental antiandrogens affect reproductive development and play behavior in the Sprague-Dawley rat.

Hotchkiss

Ostby

VanDenburgh

et al. 2002

Environ Health Perspect

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In mammals, exposure to androgens early in development is essential for masculinization of the male reproductive phenotype. Male fetuses exposed to antiandrogens during perinatal life are permanently demasculinized in their morphology and physiology, whereas exposure to exogenous androgens permanently masculinizes females. In some litter-bearing species, proximity in utero of females to males can partially masculinize female siblings and alter their responsiveness to endocrine-disrupting compounds. However, in our strain of rat (CD-SD Charles River), intrauterine position does not significantly influence testosterone concentrations and anogenital distance of fetuses. In comparison, administration of testosterone propionate to pregnant females, at doses that doubled fetal female testosterone levels, did masculinize the reproductive system. Discovery of androgen-active chemicals in the environment has placed increased emphasis on describing the reproductive and behavioral effects of both natural and environmental androgens and antiandrogens. Recently, the effects of an antiandrogen, vinclozolin, on the brain and behavior were cited as a special concern by the U.S. Environmental Protection Agency in its risk assessment of this pesticide. In rats, one such behavior that is perinatally organized by androgens is social play. Males play more than females, and administration of exogenous androgens during the neonatal period alters the juvenile expression of this sexually dimorphic behavior. Vinclozolin is an androgen receptor antagonist that inhibits androgen-dependent tissue growth in vivo. We were interested in whether developmental exposure to vinclozolin could also alter androgen-dependent behaviors such as play. Neonatal male rats were injected on postnatal days (PNDs) 2 and 3 with corn oil, the pharmacologic antiandrogen flutamide (50 mg/kg), or vinclozolin (200 mg/kg). On PNDs 36-37 animals were observed for social play. Behaviors associated with general social activity such as sniffing and dorsal contact were unaffected by treatment. However, play behavior in males treated with flutamide or vinclozolin was significantly reduced, resembling levels of play characteristic of females rather than untreated males. Therefore, this study demonstrates that perinatal exposure to vinclozolin, an environmental antiandrogen, can alter androgen-dependent play behavior in the male rat.

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Concentrations of testosterone and androsterone in peripheral and umbilical venous plasma of fetal rats

Cited by 20 publications

References 17 publications

The masculinization of the fetus during pregnancy due to inhalation of diesel exhaust.

The masculinization of the fetus during pregnancy due to inhalation of diesel exhaust.

Plasma testosterone in fetal rats and their mothers on day 19 of gestation

Androgens and environmental antiandrogens affect reproductive development and play behavior in the Sprague-Dawley rat.

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