Disruption of thyroid hormone-mediated Xenopus laevis tadpole tail tip regression by hexabromocyclododecane (HBCD) and 2,2′,3,3′,4,4′,5,5′,6-nona brominated diphenyl ether (BDE206)

Thyroid hormone regulates amphibian metamorphosis, including the transformation of a tadpole into a froglet and regression of the tail. Xenopus laevis tadpole tail tips in organ culture (ex vivo) undergo regression when exposed to 3,3′,5-triiodo-l-thyronine (T3) and interference by chemicals with this process was utilized as a bioassay to detect thyroid hormone disruption. In the present study the bioassay was further validated by investigating its response to compound induced T3-antagonism and – potentiation. Tadpole tail tips were exposed to two brominated flame retardants (BFRs) in presence or absence of T3 at its EC50 (20 nM). T3-induced tail tip regression was antagonized by 2,2′,3,3′,4,4′,5,5′,6-nona brominated diphenyl ether (BDE206) and potentiated by hexabromocyclododecane (HBCD) in a concentration dependent manner, which was consistent with results obtained with a in vitro T3-dependent proliferation bioassay termed the T-screen. Neither compound induced any effect in the absence of T3. The results indicate that studying possible hormone disrupting effects of agonistic, antagonistic or potentiating compounds should include combined exposure with the natural hormone at around its EC50 concentration. The results obtained with the tail tip exposures were in accordance with the T-screen predictions, and occurred at BFR-concentrations that were only 5–50 times those of T3. The bioassay proved to be suitable not only for detecting T3-agonism, but also for antagonism and potentiation.