4.7 Article

Short-Term Exposure Effects of the Environmental Endocrine Disruptor Benzo(a)Pyrene on Thyroid Axis Function in Zebrafish

期刊

出版社

MDPI
DOI: 10.3390/ijms23105833

关键词

zebrafish; hypothalamic-pituitary-thyroid axis; endocrine disruptor chemicals; benzo(a)pyrene; central hypothyroidism

资金

  1. Italian Ministry of Health, Rome, Italy [2765253]
  2. Italian Ministry of University and Research (MUR), Rome Italy (Program PRIN 2017) [2017TK7Z8L]
  3. program of Promising Young Researchers of the University of Milan

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In this study, the effects of BaP on thyroid development and function were tested using zebrafish as a model system. The results showed that exposure to BaP significantly affects thyroid function in zebrafish, with the primary toxic effects occurring at the hypothalamic-pituitary level, creating a model of central hypothyroidism.
Benzo(a)Pyrene (BaP) is one of the most widespread polycyclic aromatic hydrocarbons (PAHs) with endocrine disrupting properties and carcinogenic effects. In the present study, we tested the effect of BaP on thyroid development and function, using zebrafish as a model system. Zebrafish embryos were treated with 50 nM BaP from 2.5 to 72 h post fertilization (hpf) and compared to 1.2% DMSO controls. The expression profiles of markers of thyroid primordium specification, thyroid hormone (TH) synthesis, hypothalamus-pituitary-thyroid (HPT) axis, TH transport and metabolism, and TH action were analyzed in pools of treated and control embryos at different developmental stages. BaP treatment did not affect early markers of thyroid differentiation but resulted in a significant decrease of markers of TH synthesis (tg and nis) likely secondary to defective expression of the central stimulatory hormones of thyroid axis (trh, tshba) and of TH metabolism (dio2). Consequently, immunofluorescence of BaP treated larvae showed a low number of follicles immunoreactive to T4. In conclusion, our results revealed that the short-term exposure to BaP significantly affects thyroid function in zebrafish, but the primary toxic effects would be exerted at the hypothalamic-pituitary level thus creating a model of central hypothyroidism.

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