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EXPOSURE PARAMETERS FOR DELAYED PUBERTY AND MAMMARY GLAND DEVELOPMENT IN LONG-EVANS RATS EXPOSED IN UTERO TO ATRAZINE
Citation:
Rayner, J. L. AND S E. Fenton. EXPOSURE PARAMETERS FOR DELAYED PUBERTY AND MAMMARY GLAND DEVELOPMENT IN LONG-EVANS RATS EXPOSED IN UTERO TO ATRAZINE. Presented at Society of Toxicology, Salt Lake City, UT, March 09 - 13, 2003.
Description:
Exposure Parameters For Delayed Puberty And Mammary Gland Development In Long-Evans Rats Exposed In Utero To Atrazine
Jennifer L. Rayner1 and Suzanne E. Fenton2
1 UNC-Chapel Hill, DESE, Chapel Hill, NC, and 2 RTD, USEPA, NHEERL/ORD, RTP,NC
Prenatal exposure to the herbicide atrazine (ATR) was found to delay vaginal opening (VO) in the offspring of Long-Evans (LE) rats. Our preliminary studies suggested that ATR exposure also delayed mammary development in LE female offspring. To evaluate ATR exposure parameters for pubertal and mammary gland development delays, we asked whether ATR-induced delays were strictly dam-mediated (via milk) or a direct effect (transplacental) on the pups. Timed-pregnant LE rats (N=20/group) were gavaged gestational days 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 (birth-milk source, respectively). BW was compared on PND4, PND22, day of VO, and PND60. Pup BW was significantly reduced on PND4 for all groups exposed to ATR vs. C-C, but was no longer different among the dose groups at weaning. On PND40 and 60 serum luteinizing and prolactin levels did not vary between groups. Serum thyroid stimulating hormone was slightly elevated in the ATR-ATR group on PND60, but not PND40 (p<0.05). A significant delay in VO and increase in VO BW was seen only in the litters receiving milk from ATR-treated dams (MeanVO +SE, N>8 litters/group); C-C 33.3 +0.6d, ATR-C 33.8 +1.1d, C-ATR 35.1 +0.9d, and ATR-ATR 37.0 +0.7d. Following developmental scoring, mammary glands of female offspring (2/dam) in groups ATR-C, C-ATR, and ATR-ATR displayed significant delays in epithelial development on PNDs4, 33, and 40. However, at all ages examined, ATR-ATR offspring exhibited the least developed glands. Our data suggests that the delay in VO of in utero ATR-exposed offspring is mediated via the dam [milk], and does not appear to be influenced by offspring BW or direct exposure to ATR in utero. However, delays in mammary gland development appear to be the result of direct and/or suckling exposure parameters. (This is an abstract of a proposed presentation and does not necessarily reflect EPA policy; Supported by NHEERL-DESE, EPA CT826513, and NSF, No. HRD-9978874)