Reduced thyroxine levels in mice perinatally exposed to polybrominated diphenyl ethers

• Published in: Environmental toxicology and pharmacology 2005-02, Vol.19 (2), p.273-281
• Main Authors: Skarman, Ellen, Darnerud, Per Ola, Öhrvik, Helena, Oskarsson, Agneta
• Format: Article
• Language: English
• Subjects: BDE-99; Bromkal; Endocrine disruptor; PBDEs; Polybrominated diphenyl ethers; Thyroxine
• ISSN: 1382-6689; 1872-7077
• DOI: 10.1016/j.etap.2004.08.001

The aim of the study was to follow plasma thyroxine levels and hepatic enzyme activities in offspring after maternal gestational and lactational exposure to polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls. Mice were given 10 equimolar oral doses from gestational day (GD) 4 to postnatal day (PND) 17 of either Bromkal 70-5DE, 2,2′,4,4′,5-pentabrominated diphenyl ether (BDE-99) or Aroclor 1254 (total dose of 0.80 mmol/kg, b.w.). Plasma thyroxine levels were reduced in offspring in the Aroclor and Bromkal groups on PND11 but had returned to control levels by PND37. No effects on thyroxine levels were seen in the dams. Hepatic activity of EROD was increased in all treated offspring groups and so was UDP-GT in Aroclor-exposed offspring on PND11 and PND18. This study shows that PBDEs and PCBs, probably after microsomal transformation, have endocrine disrupting properties in perinatally exposed juvenile mice, most pronounced at PND11. However, BDE-99 had no effect on thyroxine levels, suggesting that other components in Bromkal are responsible for the hypothyroxinemia.