Developmental exposure to decabromodiphenyl ether (PBDE 209): Effects on thyroid hormone and hepatic enzyme activity in male mouse offspring

Abstract

Decabrominated diphenyl ether (PBDE 209) is the second most used brominated flame retardant (BFRs). Many studies have shown that some of the BFRs act as endocrine disruptors via alterations in thyroid hormone homeostasis and affect development. Little is known about the effect of prenatal exposure to PBDE 209 on the development in male offspring. Using a CD-1 mouse model, we attempt to estimate the possible effect of in utero exposure to PBDE 209 on thyroid hormone and hepatic enzymes activities in male offspring. Pregnant mice were administered different doses of PBDE 209 (10, 500, and 1500 mg/kg/day) or corn oil for controls per gavage from gestational days 0–17. In adult male offspring whose mothers had been treated with 1500 mg/kg of PBD 209, hepatic enzyme activity of S9 7-ethoxyresorufin O-deethylase (EROD) was weak but significantly increased (54%). However, no significant changes were observed in S9 4-nitrophenol uridinediphosphate-glucuronosyltransferase (UDPGT) in any of the treatment groups. Serum triiodothyronine (T3) was found to have decreased significantly (ca. 21% both 10 mg/kg and 1500 mg/kg) in offspring, but not thyroxine (T4). Histopathological examination revealed that prenatal exposure of PBDE 209 might be related with cell swelling of hepatocytes in male offspring and there were mild changes in the thyroid glands in 1500 mg/kg group. These data demonstrate that PBDE 209 is likely an endocrine disrupter in male mice following exposure during development. Further studies using environmentally relevant doses are needed for hazard identification.