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.