Inhibition of vitellogenin gene induction by 2,3,7,8-tetrachlorodibenzo-p-dioxin is mediated by aryl hydrocarbon receptor 2 (AHR2) in zebrafish (Danio rerio)

► Induction of vitellogenins 1–3 are inhibited by 2,3,7,8-TCDD and 1,2,3,7,8-PeCDD. ► The AHR2 mediates the cross-talk inhibition of vitellogenin expression in zebrafish. ► The zebrafish bioassay will be useful for probing mechanisms of endocrine disruption. ► These studies provide insight into repr...

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Published in:Aquatic toxicology 2013-01, Vol.126 (15), p.1-8
Main Authors: Bugel, Sean M., White, Lori A., Cooper, Keith R.
Format: Article
Language:English
Subjects:
Agnatha. Pisces
agonists
AHR–ER cross-talk
Animal, plant and microbial ecology
Animals
Applied ecology
bioassays
Biological and medical sciences
Danio rerio
Dioxin
Dioxins - toxicity
Ecotoxicology, biological effects of pollution
Effects of pollution and side effects of pesticides on vertebrates
Endocrine disruption
Estrogens - pharmacology
Ethinyl Estradiol - pharmacology
Fish reproduction
Freshwater
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Developmental - drug effects
gene induction
Gene Knockdown Techniques
genes
Morpholinos - genetics
pollutants
Polychlorinated Dibenzodioxins - toxicity
pretreatment
Receptors, Aryl Hydrocarbon - genetics
Receptors, Aryl Hydrocarbon - metabolism
Teleostei
Vitellogenesis
vitellogenin
Vitellogenins - genetics
Vitellogenins - metabolism
Water Pollutants, Chemical - toxicity
Zebrafish
Zebrafish - embryology
Zebrafish - genetics
Zebrafish Proteins - genetics
Zebrafish Proteins - metabolism
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Summary:► Induction of vitellogenins 1–3 are inhibited by 2,3,7,8-TCDD and 1,2,3,7,8-PeCDD. ► The AHR2 mediates the cross-talk inhibition of vitellogenin expression in zebrafish. ► The zebrafish bioassay will be useful for probing mechanisms of endocrine disruption. ► These studies provide insight into reproductive effects in species exposed to dioxins. Vitellogenins are hepatically derived yolk-protein precursors required for oogenesis in all oviparous teleosts. Altered gene-regulation of vitellogenesis by environmental contaminants can have profound effects on reproductive success, and ultimately population sustainability. To better understand chemical effects on vitellogenin gene regulation, we tested the hypothesis that activation of the aryl hydrocarbon receptor 2 (AHR2) by dioxin inhibits the estrogen receptor pathway regulation of 3 vitellogenin genes (vtg1–3) in vivo, using zebrafish (Danio rerio) as a model teleost. Using an embryo–larval bioassay, embryos were either treated with 1000pptr (parts-per-trillion, pg/mL) 17α-ethynylestradiol (EE2) alone from 6h post fertilization (hpf) to 4 days post fertilization (dpf), or pre-treated with dioxin (4–5hpf) prior to EE2. Pre-treatment with 400pptr 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) or 1,2,3,7,8-pentachlorodibenzo-p-dioxin inhibited the EE2 induction of vtg1, vtg2 and vtg3 by >95% (p≤0.05). In comparison, a splice-blocking AHR2 morpholino used to down-regulate ahr2 expression significantly reduced the inhibition of vtg1, vtg2 and vtg3 by 400pptr 2,3,7,8-TCDD (20.7–27.4% rescue). These studies demonstrate that 2,3,7,8-TCDD directly inhibits the vitellogenin pathway in vivo through activation of the AHR2. This work provides evidence for AHR2 dependent cross-talk inhibition of vitellogenin genes and offers insight into anti-estrogenic reproductive effects observed in oviparous species exposed to AHR agonist contaminants.
ISSN:0166-445X
1879-1514
DOI:10.1016/j.aquatox.2012.09.019