The effects of perchlorate on thyroidal gene expression are different from the effects of iodide deficiency.

Perchlorate (ClO₄⁻), which is a ubiquitous and persistent ion, competitively interferes with iodide (I) accumulation in the thyroid, producing I deficiency (ID), which may result in reduced thyroid hormone synthesis and secretion. Human studies suggest that ClO₄⁻ presents little risk in healthy individuals; however, the precautionary principle demands that the sensitive populations of ID adults and mothers require extra consideration. In an attempt to determine whether the effects on gene expression were similar, the thyroidal effects of ClO₄⁻ (10 mg/kg) treatment for 14 d in drinking water were compared with those produced by 8 wk of ID in rats.

A method for the analysis of six thyroid hormones in thyroid gland by liquid chromatography-tandem mass spectrometry.

Perchlorate can competitively inhibit iodide uptake by the thyroid gland (TG) via the sodium/iodide symporter, consequently reducing the production of thyroid hormones (THs). Until recently, the effects of perchlorate on TH homeostasis are being examined through measurement of serum levels of TH, by immunoassay (IA)-based methods. IA methods are fast, but for TH analysis, they are compromised by the lack of adequate specificity.