Accumulation and debromination of decabromodiphenyl ether (BDE-209) in juvenile fathead minnows (Pimephales promelas) induces thyroid disruption and liver alterations.

Polybrominated diphenyl ether (PBDE) flame retardants are known to affect thyroid hormone (TH) regulation. The TH-regulating deiodinases have been implicated in these impacts; however, PBDE effects on the fish thyroid system are largely unknown. Moreover, the liver as a potential target of PBDE toxicity has not been explored in young fish. This study measured decabromodiphenyl ether (BDE-209) effects on TH regulation by measuring deiodinase activity in juvenile fathead minnows (Pimephales promelas). Dietary accumulations and debromination of BDE-209 were also measured, and the morphology of thyroid and liver tissues was examined. Juvenile fathead minnows (28 days old) received a 28-day dietary treatment of BDE-209 at 9.8 ± 0.16 μg/g of food at 5% of their body weight per day followed by a 14-day depuration period in which they were fed clean food. Chemical analysis revealed that BDE-209 accumulated in tissues and was metabolized to reductive products ranging from penta- to octaBDEs with 2,2',4,4',5,6'-hexabromodiphenyl ether (BDE-154) being the most accumulative metabolite. By day 28 of the exposure, rates of outer and inner ring deiodination (ORD and IRD, respectively) of thyroxine (T4) were each reduced by ∼74% among treatments. Effects on T4-ORD and T4-IRD remained significant even after the 14-day depuration period. Histological examination of treated fish showed significantly increased thyroid follicular epithelial cell heights and vacuolated hepatocyte nuclei. Enlarged biliary passageways may be the cause of the distinctive liver phenotype observed, although further testing is needed. Altogether, these results suggest that juvenile fish may be uniquely susceptible to thyroid disruptors like PBDEs.