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ToxSci Advance Access originally published online on June 2, 2005
Toxicological Sciences 2005 87(1):255-266; doi:10.1093/toxsci/kfi213
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© The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Adverse Effects of Prenatal Exposure to Atrazine During a Critical Period of Mammary Gland Growth

Jennifer L. Rayner*,{dagger}, Rolondo R. Enoch{dagger},2 and Suzanne E. Fenton{dagger},1

* Department of Environmental Sciences and Engineering, School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599; {dagger} Reproductive Toxicology Division, Office of Research and Development, National Health & Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711

Received March 22, 2005; accepted May 26, 2005

Prenatal exposure to 100 mg/kg atrazine (ATR) delays mammary gland (MG) development in resulting female offspring of Long-Evans rats. To determine if the fetal MG was sensitive to ATR effects during specific periods of development, timed-pregnant dams (n = 8/group/block) were dosed for 3- or 7-gestation day (GD) intervals (GD 13–15, 15–17, 17–19, or 13–19) with 100 mg ATR/kg/day or vehicle (C), and their offspring were evaluated for changes. Mammary glands taken from pups prenatally exposed to ATR displayed significant delays in epithelial development as early as postnatal day (PND) 4 compared to C, with continued developmental delays at later time points that varied by time of exposure. However, the most persistent and severe delays were seen in the GD 17–19 and GD 13–19 ATR exposure groups, demonstrating statistically similar growth retardation. Because MG developmental deficits persisted into adulthood, we hypothesized that ATR-exposed animals may have had difficulties nursing their young. Females exposed prenatally to either ATR (as defined) or C (n = 4 litters/group) were bred, and the resulting F2 offspring from GD 17–19 and GD 13–19 exposure groups were significantly smaller in body weight (BW) than C. In a separate study, it was determined that ATR (25–100 mg/kg), delivered from GD 15–19, did not decrease fetal body weights on GD 20, even though the higher doses significantly decreased weight gain of the dosed dams. These data suggest that the consequences of brief ATR exposure during a critical period of fetal MG development (GD 17–19), are both delayed MG development of the offspring and inadequate nutritional support of F2 offspring, resulting in adverse effects on pup weight gain.

Key Words: atrazine; mammary gland; critical period; lactation.


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