Disrupted carbonic anhydrase distribution in the avian shell gland following in ovo exposure to estrogen

Eggshell thinning among wild birds has been an environmental concern for al most half a century and the underlying mechanisms are still not fully under stood. Previously we showed that exposure of quail embryos to ethynylestrad iol (EE2) caused disorganization of the tubular glands in the shell gland o f adult birds. In this study, we have examined the effect of in ovo exposur e to EE2 on carbonic anhydrase (CA) localization, especially in the shell g land, because CA is required for shell formation. In the control birds, CA was localized in the cell membranes of the tubular gland cells of the shell gland, whereas the surface epithelium was always devoid of CA. In ovo trea tment with 20 ng EE2/g egg resulted in a loss of CA activity in the tubular glands while the surface epithelium showed strong induction of both membra ne bound and cytoplasmic CA activity in 49 +/- 1% of the cells. The dose 2 ng EE2/g egg resulted in partial loss of tubular gland CA and strong induct ion of CA activity in 2.5 +/- 0.5% of the surface epithelial cells and weak er induction in 22 +/- 2% of the epithelial cells. In conclusion, this stud y shows that embryonic exposure to a xenoestrogen disrupts CA distribution in the adult shell gland. We propose that eggshell thinning in avian wildli fe could reflect a functional malformation in the shell gland, already indu ced by xenoestrogen during embryonic development rather than being caused s olely by exposure of the adult bird.