Parental exposure to 2,2′,4,4′5 - pentain polybrominated diphenyl ethers (BDE-99) causes thyroid disruption and developmental toxicity in zebrafish

Highlights: • Chronic exposure to BDE-99 in a zebrafish model was tested. • BDE-99 exposure causes thyroid endocrine disruption in the adult zebrafish. • BDE-99 exposure causes thyroid endocrine disruption and developmental toxicity in offspring larvae. -- Abstract: Although polybrominated diphenyl ethers (PBDEs) are known to disturb thyroid hormone signaling, the mechanisms underlying the effects of 2,2′,4,4′5 - pentain polybrominated diphenyl ethers (BDE-99) in fish remain unclear. In order to reveal these mechanisms, adult zebrafish (Danio rerio) were exposed to different concentrations of BDE-99 (0, 0.5, 5, or 50 μg/L) for 28 days and spawned by mating naturally in clean water (without BDE-99). Females exposed to BDE-99 showed significantly lowered thyroxine (T4) levels. Expression of transthyretin (ttr) and uridine diphosphate glucuronosyl transferase (ugt1ab) were down-regulated and up-regulated, respectively. Triiodothyronine (T3) levels in the 0.5 μg/L BDE-99 exposure group was significantly increased. Males showed significantly increased T3 levels, and lowered T4 levels, which were associated with up-regulated and down-regulated expression of deiodinase 2 (deio2) and ugt1ab, respectively. Exposure of adult zebrafish to BDE-99 lead to significantly increased T4 in the 0.5 μg/L BDE-99 exposure group, but in the 50 μg/L BDE-99 exposure group there was significantly reduced T4 in F1 larvae and altered mRNA transcription in the hypothalamic-pituitary-thyroid-liver (HPTL) axis. The offspring also showed reduced survival rates, and body length and elevated malformation rates. This study is the first in zebrafish to show that parental zebrafish exposure to BDE-99 can lead to developmental toxicity and thyroid disruption in the offspring.