Faculty Collaboration Database

In utero and lactational exposure of female Holtzman rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin: modulation of the estrogen signal. Biol Reprod 1996 Jul;55(1):62-7

Date

07/01/1996

Pubmed ID

8793059

DOI

10.1095/biolreprod55.1.62

Scopus ID

2-s2.0-0029787702 (requires institutional sign-in at Scopus site)   103 Citations

Abstract

The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) induces severe reproductive defects in male rats when exposure occurs in utero and during lactation. Yet there is currently a paucity of information regarding the effects of this exposure paradigm in females. In the current study, we examine the effects of TCDD during fetal and perinatal development on the estrogen-signaling system in peripubertal female rats. Pregnant Holtzman rats were given 1 microgram/kg TCDD or vehicle control by gavage on gestational Day 15. Body weights were reduced, though not significantly, on postnatal Day 21. While ovarian and uterine wet weights were not increased by TCDD exposure, the percentage of body weight attributed to the ovary was increased significantly. Through use of ribonuclease protection and gel-shift assays, exposed females were compared with nonexposed counterparts for estrogen receptor (ER) mRNA and DNA-binding activity in the following tissues: hypothalamus, pituitary (mRNA only), uterus, and ovary. ER mRNA levels increased in the hypothalamus, uterus, and ovary, and decreased in the pituitary. The results of the DNA-binding assays paralleled the mRNA results in the uterus, while DNA-binding activity was decreased in the hypothalamus and was unchanged in ovarian protein extracts. Circulating concentrations of estrogen were significantly lower in TCDD-exposed rats than in controls. These data suggest that the decrease in serum estrogen may be a cause of the alterations in ER mRNA; the changes in ER DNA-binding activity may indicate alterations in either translation or posttranslational receptor processing. Overall, this study shows that TCDD may act systemically in this model, and these effects should not necessarily be characterized as antiestrogenic.

Author List

Chaffin CL, Peterson RE, Hutz RJ

Author

Reinhold J. Hutz in the Biological Sciences department at University of Wisconsin - Milwaukee

MESH terms used to index this publication - Major topics in bold

Animals
Base Sequence
Body Weight
DNA
Estrogens
Female
Hypothalamus
Lactation
Male
Ovary
Pituitary Gland
Polychlorinated Dibenzodioxins
Pregnancy
Prenatal Exposure Delayed Effects
RNA, Messenger
Rats
Rats, Sprague-Dawley
Receptors, Estrogen
Uterus