Department of Biomedical Sciences and Veterinary Public Health, Swedish University of Agricultural Sciences, PO Box 7078, SE-75007 Uppsala, Sweden.
Environ Toxicol Pharmacol. 2005 Feb;19(2):273-81. 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 0.80mmol/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.
本研究旨在观察母体妊娠期和哺乳期暴露于多溴联苯醚（PBDEs）和多氯联苯（PCBs）后，仔鼠血浆甲状腺素水平和肝酶活性的变化。实验中，从妊娠第 4 天（GD）到产后第 17 天（PND），给小鼠经口给予 10 个等摩尔剂量的 Bromkal 70-5DE、2,2',4,4',5-五溴联苯醚（BDE-99）或 Aroclor 1254，总剂量为 0.80mmol/kg.b.w.。结果显示，在 PND11 时，Aroclor 和 Bromkal 组的仔鼠血浆甲状腺素水平降低，但到 PND37 时已恢复至对照水平。母鼠的甲状腺素水平无变化。在所有处理组的仔鼠中，肝组织 EROD 活性均升高，而 Aroclor 暴露组的仔鼠在 PND11 和 PND18 时 UDP-GT 活性也升高。该研究表明，PBDEs 和 PCBs 可能在经胎盘暴露的幼鼠中具有内分泌干扰特性，在 PND11 时最为明显。然而，BDE-99 对甲状腺素水平没有影响，提示 Bromkal 中的其他成分是导致低甲状腺素血症的原因。
