Cl. Chaffin et al., ALTERATIONS TO THE PITUITARY-GONADAL AXIS IN THE PERIPUBERTAL FEMALE RAT EXPOSED IN-UTERO AND THROUGH LACTATION TO 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN, Biology of reproduction, 56(6), 1997, pp. 1498-1502
The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD;
dioxin) is a potent disrupter of vertebrate endocrine systems. It was
shown previously that in utero and lactational (IUL) exposure to TCDD
resulted in a reduction in serum estradiol concentrations; however, t
he mechanism for this remains unknown. In the current study, the effec
ts of perinatal exposure to TCDD on the pituitary-ovarian axis were ex
amined. Pregnant rats were given a single oral dose of 1 mu g TCDD/kg
or vehicle as control on gestation Day 15, and female pups were killed
on postnatal Day 21. Pituitaries were assayed for gonadotropin beta-s
ubunit mRNA; additional pituitaries were cultured for 4 h and the medi
a were assayed for FSH. Gonadotropin receptor mRNAs from vehicle- and
TCDD-exposed animals were compared, with some ovaries cultured and the
media assayed for estrogen secretion. LH, FSH, progesterone, and andr
ostenedione concentrations were determined in serum. IUL exposure to T
CDD resulted in a significant reduction of pituitary FSH beta mRNA. Al
though estrogen output was shown to be reduced, neither serum FSH nor
LH concentration was increased significantly, and FSH secretion in vit
ro was not altered. Similarly, serum progesterone and androstenedione
were not altered by TCDD exposure, while in vitro estrogen secretion w
as significantly reduced. These data suggest that TCDD did not act on
serum gonadotropin concentrations. The reduction in the concentration
of serum estrogen appears to result from direct or indirect actions on
the ovary at some point following androstenedione production.