PMID- 12798966
OWN - NLM
STAT- MEDLINE
DCOM- 20030728
LR  - 20190922
IS  - 0892-0362 (Print)
IS  - 0892-0362 (Linking)
VI  - 25
IP  - 4
DP  - 2003 Jul-Aug
TI  - Dietary ethinyl estradiol exposure during development causes increased voluntary 
      sodium intake and mild maternal and offspring toxicity in rats.
PG  - 491-501
AB  - Exogenous estrogen exposure during development often results in behavioral 
      masculinization and/or defeminization of genetic females. Genetic males may be 
      defeminized, hypermasculinized or even demasculinized after similar treatment. 
      Here, pregnant Sprague-Dawley rats consumed phytoestrogen-free diets containing 
      0, 1, 5 or 200 ppb EE(2) beginning on gestational day (GD) 7. Offspring were 
      weaned to the same maternal diet and maintained gonadally intact. There were mild 
      effects on body weight and food consumption in dams of the 200 ppb group and 
      their offspring weighed less at birth than those of the control group; however, 
      gross assessments of nursing behavior were normal in all dietary groups. 
      Postweaning, offspring of the 200 ppb group weighed less and consumed less food 
      than controls. There were no EE(2)-related effects on open-field activity (tested 
      at postnatal days (PND) 22-24, 43-45 and 64-66), play behavior (tested at PND 
      35), running wheel activity (PND 63-77) or intake of a 0.3% saccharin-flavored 
      solution (PND 69-71). Intake of a 3.0% sodium chloride-flavored solution on PND 
      73-75 was increased in both male and female offspring of the 200 ppb group 
      relative to same-sex controls, an effect that is reportedly estrogen mediated. 
      Sodium chloride-flavored solution intake is a sexually dimorphic behavior for 
      which female rats consume more than males. Here, while EE(2) exposure had few 
      effects on the conventional tests of sexually dimorphic behaviors, exposure to 
      200 ppb in the diet appeared to feminize genetic males and hyperfeminize genetic 
      females with regard to sodium intake.
FAU - Ferguson, Sherry A
AU  - Ferguson SA
AD  - HFT-132/Division of Neurotoxicology, National Center for Toxicological Research, 
      U.S. Food and Drug Administration, 3900 NCTR Road, Jefferson, AR 72079, USA. 
      sferguson@nctr.fda.gov
FAU - Delclos, K Barry
AU  - Delclos KB
FAU - Newbold, Retha R
AU  - Newbold RR
FAU - Flynn, Katherine M
AU  - Flynn KM
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Neurotoxicol Teratol
JT  - Neurotoxicology and teratology
JID - 8709538
RN  - 0 (Dietary Proteins)
RN  - 0 (Estradiol Congeners)
RN  - 423D2T571U (Ethinyl Estradiol)
RN  - 9NEZ333N27 (Sodium)
RN  - FST467XS7D (Saccharin)
SB  - IM
MH  - Aging/*physiology
MH  - Animals
MH  - Animals, Newborn
MH  - Behavior, Animal/*drug effects
MH  - Body Weight/drug effects
MH  - Dietary Proteins
MH  - Dose-Response Relationship, Drug
MH  - Drinking/drug effects
MH  - Eating/*drug effects
MH  - Estradiol Congeners/*toxicity
MH  - Ethinyl Estradiol/*toxicity
MH  - Exploratory Behavior/drug effects
MH  - Female
MH  - Food Preferences
MH  - Male
MH  - Motor Activity/drug effects
MH  - Pregnancy
MH  - *Prenatal Exposure Delayed Effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Saccharin
MH  - Sex Characteristics
MH  - Sodium/*metabolism
EDAT- 2003/06/12 05:00
MHDA- 2003/07/29 05:00
CRDT- 2003/06/12 05:00
PHST- 2003/06/12 05:00 [pubmed]
PHST- 2003/07/29 05:00 [medline]
PHST- 2003/06/12 05:00 [entrez]
AID - S0892036203000151 [pii]
AID - 10.1016/s0892-0362(03)00015-1 [doi]
PST - ppublish
SO  - Neurotoxicol Teratol. 2003 Jul-Aug;25(4):491-501. doi: 
      10.1016/s0892-0362(03)00015-1.