Effects of polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) on thyroid hormone and vitamin A levels in rats and mice

The ability of the commercial polybrominated diphenyl ether (PBDE) preparat ion Bromkal 70-5 DE to alter thyroid hormone and vitamin A levels as well a s microsomal enzyme activities was compared with that of the commercial pol ychlorinated biphenyl (PCB) preparation Aroclor 1254 in orally exposed fema le rats (Sprague-Dawley) and mice (C57BL/6 N). Additional mice were exposed to the PBDE congener 2,2 ' ,4,4 ' -tetrabromodiphenyl ether (DE-47). or to the PCB congener 2.3.3 ' ,4,4 ' -pentachlorobiphenyl (CB-105). For 14 days the animals were given approximately isomolar daily oral doses of Aroclor 1254. CB-105 (both 10 mg/kg body weight), Bromkal 70-5 DE or DE-47 (both at 18 mg/kg body weight). In addition, further groups of rats and mice receiv ed a higher dose of Bromkal 70-5 DE, 36 mg/kg body weight. Bromkal 70-5 DE and DE-47 decreased plasma free and total thyroxine (T4) levels in both rat s and mice. although with lower potency than that of Aroclor 1254 and CB-10 5. By contrast, thyroid-stimulating hormone (TSH) levels were not significa ntly changed in any of the groups. Reduction of hepatic vitamin A levels wa s seen in rats after Aroclor 1254 and Bromkal 70-5 DE exposure. A similar t endency was seen also in mice. but the effects were significant only for co ncentration data and not the total amount. Induction of microsomal phase I enzymes. measured as ethoxy, methoxy and pentoxy resorufin O-dealkylase (ER OD, MROD. PROD) activities. was greatest after exposure to Aroclor 1254/CB- 105 but were also significant in the Bromkal 70-5 DE/DE-47-treated groups. However, induction of uridine diphosphoglucuronosyl transferase (UDPGT) was small and for most groups insignificant. In conclusion, the PBDE compounds studied, although having a lower potency than the PCB compounds, decreased thyroxine and vitamin A levels and induced microsomal enzyme activities. R ats were more sensitive to the observed effects than mice. Microsomal phase I activity might be related, directly or indirectly, to the T4 and vitamin A effects, whereas several factors (such as weak enzyme induction and lack of correlation with altered T4 and vitamin A levels) argue against any UDP GT-related effects.