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EXPOSURE PARAMETERS NECESSARY FOR DELAYED PUBERTY AND MAMMARY GLAND DEVELOPMENT IN LONG-EVANS RATS EXPOSED IN UTERO TO ATRAZINE
Citation:
Rayner, J. L., C R. Wood, AND S E. Fenton. EXPOSURE PARAMETERS NECESSARY FOR DELAYED PUBERTY AND MAMMARY GLAND DEVELOPMENT IN LONG-EVANS RATS EXPOSED IN UTERO TO ATRAZINE. TOXICOLOGY AND APPLIED PHARMACOLOGY. Elsevier Science BV, Amsterdam, Netherlands, 195(1):23-34, (2004).
Description:
Exposure Parameters Necessary For Delayed Puberty And Mammary Gland Development In Long-Evans Rats Exposed In Utero To Atrazine
Jennifer L. Rayner1, 2, Carmen Wood2, and Suzanne E. Fenton2
1 Department of Environmental Sciences and Engineering, School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, and 2 Reproductive Toxicology Division, Office of Research and Development, National Health & Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC.
ABSTRACT
Our preliminary studies suggested that prenatal exposure to the herbicide atrazine (ATR) could delay vaginal opening (VO) and mammary development in the offspring of Long-Evans (LE) rats. To evaluate ATR exposure parameters required for pubertal delays, including mammary gland development, we used cross-fostering to determine if effects were strictly dam-mediated (via milk) or a direct effect (transplacental) on the pups. Timed-pregnant LE rats (N=20/treatment group) were gavaged gestational days (GD) 15-19 with 100 mg ATR/kg body weight (BW) or vehicle (controls, C). On PND1, half of all litters were cross-fostered, creating 4 treatment groups; C-C, ATR-C, C-ATR, and ATR-ATR (dam-milk source, respectively). A significant delay in VO and increase in VO BW was seen only in the litters receiving milk from ATR-exposed dams. However, mammary glands of female offspring (2/dam) in all groups exposed to ATR (ATR-C, C-ATR, and ATR-ATR) displayed significant delays in epithelial development. These changes were detected as early as PND4 and stunted development was evident through PND40. Further, at all developmental stages examined, offspring in the ATR-ATR group exhibited the least developed glands. These delays in pubertal endpoints do not appear to be related to body weight or endocrine hormone concentrations. Our data suggest that the delay in VO of in utero ATR-exposed offspring is mediated via the dam [milk], whereas direct exposure to ATR in utero can cause delays in mammary gland development. Our data suggest that milk-derived factors (growth factors or hormones), in addition to transplacental exposure during mammary bud outgrowth may be involved in ATR mode of action on delayed mammary gland development.