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ToxSci Advance Access published online on February 16, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfi122
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Toxicological Sciences © 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
Received November 6, 2004
Accepted February 15, 2005

Environmental Toxicology

Disruption of Thyroid Hormone Homeostasis at Weaning of Holtzman Rats by Lactational But Not in Utero Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin

Noriko Nishimura 1*, Junzo Yonemoto 1, Hisao Nishimura 2, Shin-ichi Ikushiro 3, and Chiharu Tohyama 4

1 Endocrine Disruptors and Dioxin Research Project, National Institute for Environmental Studies, Tsukuba 305-8506, Japan
2 Department of Human Sciences, Aichi Mizuho University, Toyota 470-0394, Japan
3 Graduate School of Life Science, University of Hyogo, Harima Science Garden City, Hyogo 678-1297, Japan
4 Endocrine Disruptors and Dioxin Research Project, National Institute for Environmental Studies, Tsukuba 305-8506, Japan; Environmental Health Sciences Division, National Institute for Environmental Studies, Tsukuba 305-8506, Japan

* To whom correspondence should be addressed.
Noriko Nishimura, E-mail: nishimura.noriko{at}nies.go.jp


  Abstract

The purpose of this study is to clarify whether lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is entirely responsible for the perturbation in thyroid hormone homeostasis during the neonatal period. Pregnant Holtzman rats were given a single oral dose of 1.0 µg TCDD/kg body weight on gestational day 15. Half of the litters were cross-fostered with the half of the dams treated with vehicle on postnatal day (PND) 1 to make four groups of rats, control (C/C), prenatal TCDD exposure only (T/C), postnatal TCDD exposure only (C/T), and both prenatal and postnatal TCDD exposure (T/T). On PND 21, the C/T and T/T groups, but not the T/C and C/C groups, showed a significant decrease in serum total thyroxin (TT4) and free thyroxin (FT4) concentrations in both sexes and a significant increase in serum thyroid-stimulating hormone (TSH) levels, particularly male pups. These two groups of male and female pups had significantly higher concentrations of TCDD in the liver, with marked induction of CYP1A1 mRNA and intense immunostaining of CYP1A1 in the liver. UGT1A6 and UGT1A7 mRNAs were induced in their livers, with marked immunostaining of UGT1A6. The transfer of TCDD from dams to the pups was confirmed by the detection of TCDD in mother's milk remaining in the stomachs of lactationally exposed pups on PND 1. The present results demonstrate that lactational, but not in utero, exposure to TCDD was responsible for the disruption of thyroid hormone homeostasis.

Keywords: hypothyroxinemia; lactational exposure; TCDD; thyroxin.
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