You are here:
IN UTERO EXPOSURE TO ATRAZINE INDUCES DELAYED PUBERTY OF LONG EVANS RATS: DAM-MEDIATED EFFECTS IN FEMALES
Citation:
Rayner, J. L. AND S E. Fenton. IN UTERO EXPOSURE TO ATRAZINE INDUCES DELAYED PUBERTY OF LONG EVANS RATS: DAM-MEDIATED EFFECTS IN FEMALES. Presented at Triangle Consortium for Reproductive Biology, (NIEHS)RTP, NC, February 2, 2002.
Description:
IN UTERO EXPOSURE TO ATRAZINE INDUCES DELAYED PUBERTY OF LONG EVANS RATS: DAM-MEDIATED EFFECTS IN FEMALES.
J L Rayner1 and S E Fenton2.
1 University of North Carolina at Chapel Hill, School of Public Health, Chapel Hill, NC, and 2 Reproductive Toxicology Division, USEPA, NHEERL, Research Triangle Park, NC, USA.
Exposure of Wistar dams to the common herbicide atrazine (ATR) on postnatal days (PND)1-4, will delay vaginal opening (VO) in the offspring, without reduced body weight (BW). To further evaluate ATR mode of action, we examined whether ATR-induced pubertal delays were strictly dam-mediated or a direct effect on the pups. Time pregnant Long Evans rats (N=20/group) were gavaged gestational days (GD) 15-19 with 100 mg ATR/kg or methylcellulose (controls, C). BW of the ATR dams on GD19 was significantly reduced (346 + 7g), when compared to control dams (396 + 7g). On PND1, half litters were cross-fostered, creating 4 treatment groups; C-C, C-ATR, ATR-C, and ATR-ATR (milk-birth source, respectively). BW was compared on PND4, PND22, day of VO or preputial separation (PPS), and PND60 (female) or PND120 (male). A significant delay in VO was observed in females receiving milk from ATR-treated dams (MeanSE, N>30 pups each group); C-C 33.7 + 0.4d, C-ATR 33.3 + 0.4d, ATR-C 35.4 + 0.6d, and ATR-ATR 37.1 + 0.5d. BW was significantly reduced at PND4 (N>35 pups in each group) in ATR-ATR animals vs. C-C (9%) or C-ATR (9%), but was not different between those dose groups at weaning or PND60. Although VO was delayed by ATR, the BW at VO of ATR-ATR (146.8 + 4.4) and ATR-C offspring (140.0 + 4.4) was greater than C-C (130.6 + 2.8). Male pups exposed to ATR in utero (N>18/dose group) displayed delayed PPS whether they suckled from an ATR (43.8 + 0.5d, ATR-ATR) or control dam (42.5 + 0.4, ATR-C). However, PPS was similar between C-ATR(41.5 + 0.4) and C-C (41.3 + 0.3). The ATR-ATR and ATR-C males were reduced in BW 9% and 6%, respectively, from that of C-C at PPS. Our data suggests that the delay in VO in offspring exposed to ATR in utero is mediated via the dam, and does not appear to be caused by decreased BW. Whether these effects are the result of a hormonal or lactational alteration requires further investigation. (This abstract has been reviewed in accordance with USEPA policy and approved for publication)