Prenatal transfer of decabromodiphenyl ether (BDE-209) results in disruption of the thyroid system and developmental toxicity in zebrafish offspring

- BDE-209 can accumulate in zebrafish offspring due to the exposure of parents.
- Exposure of BDE-209 to parents results in developmental toxicity in offspring.
- Disruption of the thyroid endocrine system in offspring larvae was observed after exposure of adults to BDE-209.

Decabromodiphenyl ether (BDE-209) was one of most widely-used polybrominated diphenyl ether (PBDE) flame retardants and is frequently detected in both abiotic and biotic samples from environment. However, knowledge of its transgenerational risks is limited. Here, 4-month-old zebrafish were exposed to various concentrations of BDE-209 (0, 3, 30 or 300 μg/L) for 28 days and spawned in clean water without BDE-209. Concentrations of triiodothyronine (T3) and thyroxine (T4) as well as expressions of genes involved in the hypothalamic-pituitary-thyroid (HPT) axis were measured in offspring after exposure of adult zebrafish to BDE-209. BDE-209 was accumulated in adult fish and F1 eggs, which suggests transfer of this compound from adult fish to their offspring. Exposure of BDE-209 to parents resulted in developmental abnormalities in offspring and a significant decrease in T4 concentrations in F1 larvae 120 h post-fertilization (hpf). Furthermore, expressions of several genes involved in the HPT axis were also altered. Expressions of thyroid hormone receptor α (tr-α), thyrotropin releasing hormone (trh), thyroid stimulating hormone β (tsh-β) and deiodinase 1 (dio 1) were significantly down-regulated in F1 individuals, while expressions of thyroid stimulating hormone receptor (tshr) and transthyretin (ttr) were significantly up-regulated. These results suggest that exposure of parent zebrafish to BDE-209 can cause developmental toxicity in offspring and disruption of the thyroid endocrine system of offspring.