Carcinogenesis, Vol 19, 1623-1629, Copyright © 1998 by Oxford University Press
NM Brown, PA Manzolillo, JX Zhang, J Wang and CA Lamartiniere
Prenatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was
investigated for its potential to predispose to breast cancer. Analysis of
mammary gland differentiation and cell proliferation were used as
biomarkers. Timed pregnant Sprague-Dawley CD rats were gavaged with 1
microg TCDD/kg on day 15 post-conception. Control animals were treated with
the same volume of vehicle (sesame oil) on the same schedule. Mammary gland
differentiation studies revealed that prenatal TCDD treatment, as compared
with sesame oil treatment, resulted in significantly more terminal end buds
and fewer lobules II in 50-day-old offspring, but no significant
alterations to mammary gland differentiation in 21-day-old offspring.
Terminal end buds are the most susceptible terminal ductal structures and
lobules the least susceptible to carcinogenesis. Prenatal TCDD treatment
did not alter labeling index in the mammary terminal ductal structures of
21- and 50- day-old rats, but the total proliferative compartment in
terminal end buds of 50-day-old rats was larger. Prenatal TCDD treatment
resulted in an increased number of chemically induced mammary
adenocarcinomas in rats. TCDD delayed time of vaginal opening and caused
disruption to the estrous cycle. Alteration to mammary gland
differentiation (increased number of terminal end buds) is correlated with
increased susceptibility to mammary cancer from prenatal exposure to TCDD.
ARTICLES
Prenatal TCDD and predisposition to mammary cancer in the rat
Department of Pharmacology and Toxicology, UAB Comprehensive Cancer Center, University of Alabama at Birmingham, 35294, USA.
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