The brominated flame retardant decabromodiphenyl ethane (DBDPE), an alternative to decabrominated diphenyl ether (BDE209), has become a widespread environmental contaminant, but its possible toxic effects to wildlife remain unknown. Using zebrafish as a model, we investigated the bioconcentration and impact of DBDPE on thyroid endocrine function after water-borne exposure, compared to BDE209. Zebrafish embryos were exposed to DBDPE or BDE209 (0, 3, 10, 30, 100, 300 nM) for 6 or 14 days. Chemical analysis revealed that DBDPE and BDE209 were bioconcentrated in zebrafish larvae, with similar magnitudes of accumulated concentrations. Based on screened by chromatograms, at least seven unknown compounds were observed in DBDPE-treated larvae, indicating biotransformation of the chemical. Significant increases in whole body content of triiodothyronine (T3) and thyroxine (T4) were detected in DBDPE-treated larvae, but decreased in BDE209-treated groups. Alterations in gene transcription along the related hypothalamic-pituitary-thyroid (HPT) axis were observed. Furthermore, the binding and transport protein transthyretin (TTR) was significantly increased in DBDPE exposure groups. Histological examination and stereological analysis showed no obvious pathological changes in the thyroid gland. The present study demonstrates for the first time the bioavailability, biotransformation and thyroid endocrine disruption associated with DBDPE exposure in fish. Further studies are warranted to identify the metabolites of DBDPE and to define its environmental risks to aquatic organisms.

The novel brominated flame retardant decabromodiphenyl ethane (DBDPE) has become a widespread environmental pollutant. However, the target tissue and toxicity of DBDPE are still not clear. In the current study, female zebrafish were exposed to 1 and 100 nM DBDPE for 28 days. Chemical analysis revealed that DBDPE tended to accumulate in the brain other than the liver and gonad. Subsequently, tandem mass tag-based quantitative proteomics and parallel reaction monitoring verification were performed to screen the differentially expressed proteins in the brain. Bioinformatics analysis revealed that DBDPE mainly affected the biological process related to muscle contraction and estrogenic response. Therefore, the neurotoxicity and reproductive disruptions were validated via multilevel toxicological endpoints. Specifically, locomotor behavioral changes proved the potency of neurotoxicity, which may be caused by disturbance of muscular proteins and calcium homeostasis; decreases of sex hormone levels and transcriptional changes of genes related to the hypothalamic-pituitary-gonad-liver axis confirmed reproductive disruptions upon DBDPE exposure. In summary, our results suggested that DBDPE primarily accumulated in the brain and evoked neurotoxicity and reproductive disruptions in female zebrafish. These findings can provide important clues for a further mechanism study and risk assessment of DBDPE.

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