As non-amniotes (lacking egg shells or fetal membranes as embryos) without barriers to chemical contaminants, amphibians are highly susceptible to contaminant exposure and are thus exceptionally good indicators of environmental disturbance. Even as larvae and adults, their moist permeable skin provides easy access for chemical contaminants to cross.

Frogs are the preferred amphibian model.  Frogs show responses to thyroid hormones, androgens, estrogens, and corticoids, and biological markers that can detect disturbances in all four of these hormone classes have been defined and developed.

Selecting species for amphibian assays

One major benefit of the amphibian model is the dependence of metamorphosis on proper signaling of the pituitary and thyroid. Compounds that inhibit metamorphosis could do so by interfering with any aspect of thyroid hormone synthesis, transport, receptor binding, action or degradation. Similarly, compounds that stimulate or accelerate metamorphosis can act via multiple mechanisms.

To screen chemicals for androgen agonist/antagonist activity, several assays are available. Because exogenous androgens can sex-reverse some species of amphibian larvae, by monitoring sex ratio, androgen mimics can be detected. In addition, several androgen-dependent secondary sex characters can be assayed including laryngeal size, gular pouch development, and breeding glands[47,48]. There are also several behavioral assays available to examine androgen dependent reproductive behavior and functional assays that examine fertility in males[49].

Amphibians are also useful for screening chemicals that influence estrogen levels.

Finally, because corticoids affect growth, osmoregulation, and immune function, among other aspects of amphibian development, the effects of corticoid agonists/antagonists are more complicated to assay. Often, compounds that interfere with corticoids do so by increasing or inhibiting corticoid synthesis, which is easily monitored in vivo along with the assays described above. Importantly, mechanisms other than corticoid agonism/antagonism or changes in corticoid synthesis could explain many of the effects described here [51].