Abstract
Twelve thyroid glands from free-living (n = 3) and captive (n = 9) elasmobranch fishes were investigated. Histological observation of the thyroids revealed two euthyroid glands, one case of mild chronic thyroiditis, three diffuse hyperplastic goiters, three diffuse colloid goiters, and three multinodular colloid goiters. The term goiter best describes the thyroid enlargement that results from hyperplasia and hypertrophy. Although elasmobranch goiters are typically linked to low aquatic iodine concentrations, iodine deficiency alone does not explain all of the observed thyroid conditions. Diffuse hyperplastic goiters typically result from either iodine deficiency or goitrogenic release of thyroglobulin from the follicle. Colloid goiters result from fluctuating iodine concentrations or goitrogenic agents that block the release of iodine from the thyroid gland. Although nitrate is a potential 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 appear to have similar patterns in goiter development and in the etiology of the disease.
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