Toxic effects of Decabromodiphenyl ether (BDE-209) on thyroid of broiler chicks by transcriptome profile analysis

https://doi.org/10.1016/j.ecoenv.2021.112305Get rights and content
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Highlights

  • BDE-209 exposure caused deformed and hyperplastic thyroid follicular epithelial cells.

  • Neuroactive ligand-receptor interaction was the target pathway of the BDE-209 effect.

  • Four differentially expressed receptors genes could be biomarkers of BDE-209.

  • Free triiodothyronine, thyroxine, and thyroid stimulating hormone levels were reduced.

Abstract

The wide usage of decabromodiphenyl ether (BDE-209) results in its increasing occurrence in the environment and increasing attention in regard to human and animal health. BDE-209 is an endocrine disruptor for hypothyroidism, but the toxicity mechanism is unclear. Here, the histopathology and transcriptome sequencing of thyroid tissue from broiler chicks were investigated by supplemental feeding with different concentrations of BDE-209 for 42 days (0–4 g/kg in basal diet), followed by determining the levels of thyroid hormones in serum. The results showed ruptured and even hyperplastic follicular epithelial cells in the thyroid, and a total of 501 differentially expressed genes were screened out: 222 upregulated and 279 downregulated. Based on the Kyoto Encyclopedia of Genes and Genomes database, neuroactive ligand-receptor interaction pathway was significantly enriched, and α1D-adrenergic receptor, follicle-stimulating hormone receptor, thyroid stimulating hormone receptor, and somatostatin receptor type 2 were shown to be candidate biomarkers. Thyroxine was a possible biomarker due to clear reduction in serum and significant correlation with exposure concentrations. These results suggested that oral intake of BDE-209 can cause structural injuries and even hyperplasia, and affect gene transcription involved in the neuroactive ligand-receptor interaction pathway of thyroid, as well as thyroid hormones in serum.

Keywords

Broiler chicks
Decabromodiphenyl ether
Histopathology
Thyroid hormones
Transcriptome analysis

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