Twelve thyroid glands from free-living (n = 3) and captive (n = 9) elasmobr
anch fishes were investigated. Histological observation of the thyroids rev
ealed two euthyroid glands, one case of mild chronic thyroiditis, three dif
fuse hyperplastic goiters, three diffuse colloid goiters, and three multino
dular colloid goiters. The term goiter best describes the thyroid enlargeme
nt that results from hyperplasia and hypertrophy. Although elasmobranch goi
ters are typically linked to low aquatic iodine concentrations, iodine defi
ciency alone does not explain all of the observed thyroid conditions. Diffu
se hyperplastic goiters typically result from either iodine deficiency or g
oitrogenic release of thyroglobulin from the follicle. Colloid goiters resu
lt from fluctuating iodine concentrations or goitrogenic agents that block
the release of iodine from the thyroid gland. Although nitrate is a potenti
al goitrogenic agent in aquaria, research indicates that nitrate interferes
with the uptake and retention of iodide. This interference is not directly
related to iodide storage in colloid goiters. Elasmobranchs and humans app
ear to have similar patterns in goiter development and in the etiology of t
he disease.