Chen Yu, Sible Jill C, McNabb F M Anne
Department of Biological Sciences, 2119 Derring Hall, Virginia Polytechnic Institute and State University, Virginia Tech, Blacksburg, VA 24061-0406, USA.
Gen Comp Endocrinol. 2008 Nov-Dec;159(2-3):196-207. doi: 10.1016/j.ygcen.2008.08.014. Epub 2008 Sep 6.
Perchlorate, a known thyroid disruptor, is deposited in eggs of exposed female birds, raising concerns that the embryos from these eggs may become hypothyroid, which may in turn affect the development and function of thyroid-dependent organs. We hypothesized that exposure to ammonium perchlorate (AP) would decrease hen and embryonic thyroid function and affect the expression of thyroid-responsive genes in embryonic brain and liver. Laying Japanese quail hens were treated with 2000 mg/l or 4000 mg/l AP in drinking water. Thyroid status and expression of thyroid-responsive genes were examined in the embryos from eggs of exposed hens. Perchlorate exposure led to hypothyroidism in hens from both treatment groups; egg production was decreased in the high dosage group only. Embryos from eggs of perchlorate-exposed hens had hypertrophied thyroid glands and significantly lower thyroidal hormone storage, indicating hypothyroidism in these embryos. The embryonic hypothyroidism was associated with decreased embryonic growth, delayed hatching and greater mortality during hatching. The mRNA level of type 2 deiodinase (D2) in the liver of embryos from eggs of perchlorate-exposed hens was increased compared to the control embryos, a compensatory response that increases the production of metabolically active T(3). However, the mRNA levels of D2 and RC3 in the brain were not affected. These results suggest that the embryonic brain is protected from hypothyroidism by other mechanisms known to influence hormone entry into and exit from the brain. Our study shows that maternal perchlorate exposure led to embryonic hypothyroidism and may have interfered with embryonic development.
高氯酸盐是一种已知的甲状腺干扰物，会沉积在暴露于该物质的雌性鸟类的蛋中，这引发了人们对这些蛋中的胚胎可能会出现甲状腺功能减退的担忧，而这反过来可能会影响甲状腺依赖器官的发育和功能。我们假设，暴露于高氯酸铵（AP）会降低母鸡和胚胎的甲状腺功能，并影响胚胎大脑和肝脏中甲状腺反应基因的表达。将产蛋的日本鹌鹑母鸡的饮用水中添加2000毫克/升或4000毫克/升的AP。对暴露母鸡所产蛋的胚胎进行甲状腺状态和甲状腺反应基因表达的检测。两个处理组的母鸡暴露于高氯酸盐后均出现甲状腺功能减退；仅高剂量组的产蛋量下降。暴露于高氯酸盐的母鸡所产蛋的胚胎甲状腺肿大，甲状腺激素储备显著降低，表明这些胚胎存在甲状腺功能减退。胚胎甲状腺功能减退与胚胎生长减缓、孵化延迟和孵化期间死亡率增加有关。与对照胚胎相比，暴露于高氯酸盐的母鸡所产蛋的胚胎肝脏中2型脱碘酶（D2）的mRNA水平升高，这是一种代偿反应，可增加代谢活性T(3)的产生。然而，大脑中D2和RC3的mRNA水平未受影响。这些结果表明，胚胎大脑通过其他已知影响激素进出大脑的机制来免受甲状腺功能减退的影响。我们的研究表明，母体暴露于高氯酸盐会导致胚胎甲状腺功能减退，并可能干扰胚胎发育。
