Effects of larval exposure to estradiol on spermatogenesis and in vitro gonadal steroid secretion in African clawed frogs, Xenopus laevis.

Estrogen or eco-estrogenic chemicals can disrupt normal gonadal sex differentiation, causing intersex formation and feminization in amphibians. The cellular basis for estrogen-induced sex reversal is not well understood. In the present study, we investigated the concentration- and stage-dependent effects of estradiol (E(2)) exposure during the larval period on histological characteristics of gonadal sex differentiation and gonadal sex steroid secretion in vitro in the African clawed frog, Xenopus laevis. Embryos were exposed to E(2) (1, 10, or 100 microg/L) or vehicle control through metamorphosis and then allowed to develop in untreated medium for 2-mo post-metamorphosis. To investigate gonadal sex differentiation and development during and after exposure, gonadal samples were collected at different developmental stages. Gonadal sex differentiation did not occur before NF stage 52 in any group. At NF stage 54-55 primordial germ cells (PGCs) were observed in both cortical and medullary regions of developing tadpoles gonads in the control, 1 and 10 microg/L E(2) treatments, but were observed only in the cortical region of tadpoles exposed to 100 microg/L E(2). E(2) increased the percent of spermatocytes, spermatids, and spermatozoa compared to controls. Larval E(2) exposure did not alter hCG-induced gonadal testosterone secretion in vitro but significantly increased E(2) secretion from ovaries of juvenile frogs. Our results indicate that E(2) exposure during larval development appears to prevent PGC migration to the medulla of developing gonads in a concentration-dependent manner. The degree of PGC migration to the medulla may be related to the degree of E(2)-induced intersex formation and feminization in X. laevis. E(2) exposure during the larval period accelerates spermatogenesis and can increase ovarian E(2) secretion in juvenile frogs.