Effects of maternal exposure to ammonium perchlorate on thyroid function and the expression of thyroid-responsive genes in Japanese quail embryos.

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.