Altered thyroxin and retinoid metabolic response to 2,3,7,8-tetrachlorodibenzo-p-dioxin in aryl hydrocarbon receptor-null mice

To determine whether the disruption of thyroid hormone and retinoid homeostasis that occurs after exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can be mediated by the arylhydrocarbon receptor (AhR), pregnant AhR-heterozygous (AhR+/-) mice were administered a single oral dose of 10 microg kg...

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Veröffentlicht in:Archives of toxicology 2005-05, Vol.79 (5), p.260-267
Hauptverfasser: NISHIMURA, Noriko, YONEMOTO, Junzo, MIYABARA, Yuichi, FUJII-KURIYAMA, Yoshiaki, TOHYAMA, Chiharu
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container_start_page 260
container_title Archives of toxicology
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creator NISHIMURA, Noriko
YONEMOTO, Junzo
MIYABARA, Yuichi
FUJII-KURIYAMA, Yoshiaki
TOHYAMA, Chiharu
description To determine whether the disruption of thyroid hormone and retinoid homeostasis that occurs after exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can be mediated by the arylhydrocarbon receptor (AhR), pregnant AhR-heterozygous (AhR+/-) mice were administered a single oral dose of 10 microg kg(-1) TCDD at gestation day 12.5. Serum and liver were collected on postnatal day 21 from vehicle-treated control or TCDD-treated AhR+/- and AhR-null (AhR-/-) mouse pups. Whereas TCDD exposure resulted in a marked reduction of total thyroxin (TT4) and free T4 (FT4) levels in the serum of AhR+/- mice, TCDD had no effects on AhR-/- mice. Gene expression of UDP-glucuronosyltransferase (UGT)1A6, cytochrome P450 (CYP)1A1, and CYP1A2 in the liver was induced markedly by TCDD in AhR+/- but not AhR-/- mice. Induction of CYP1A1 in response to TCDD was confirmed by immunohistochemical evidence in that CYP1A1 protein was conspicuously localized in the cytoplasm of hepatocytes in the centrilobular region. Levels of retinyl palmitate were greatly reduced in the liver of TCDD-exposed AhR+/- mice, but not in vehicle-treated AhR+/- mice. No effects of TCDD on retinoid levels in the liver were found in AhR-/- mice. We conclude that disruption of thyroid hormone and retinoid homeostasis is mediated entirely via AhR. Induction of UGT1A6 is thought to be responsible at least partly for reduced serum thyroid hormone levels in TCDD-exposed mice.
doi_str_mv 10.1007/s00204-004-0626-4
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Induction of UGT1A6 is thought to be responsible at least partly for reduced serum thyroid hormone levels in TCDD-exposed mice.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>15902423</pmid><doi>10.1007/s00204-004-0626-4</doi><tpages>8</tpages></addata></record>
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subjects Administration, Oral
Animals
Animals, Newborn
Biological and medical sciences
Cytochrome P-450 CYP1A1 - biosynthesis
Cytochrome P-450 CYP1A1 - genetics
Cytochrome P-450 CYP1A2 - biosynthesis
Cytochrome P-450 CYP1A2 - genetics
Environmental Pollutants - toxicity
Enzyme Induction
Female
Fluorescent Antibody Technique, Indirect
Gene Expression Regulation, Enzymologic - drug effects
Glucuronosyltransferase - biosynthesis
Glucuronosyltransferase - genetics
Homeostasis
Immunoenzyme Techniques
Liver - drug effects
Liver - enzymology
Male
Maternal Exposure
Medical sciences
Mice
Mice, Inbred C57BL
Mice, Knockout
Polychlorinated Dibenzodioxins - toxicity
Pregnancy
Receptors, Aryl Hydrocarbon - deficiency
Receptors, Aryl Hydrocarbon - genetics
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - metabolism
Rodents
Thyroid gland
Thyroxine - blood
Toxicology
Vitamin A - metabolism
title Altered thyroxin and retinoid metabolic response to 2,3,7,8-tetrachlorodibenzo-p-dioxin in aryl hydrocarbon receptor-null mice
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