Study of potential inhibitors of thyroid iodide uptake by using CHO cells stably expressing the human sodium/iodide symporter (hNIS) protein.
BACKGROUND
Thyroid gland is highly dependent on dietary intake of iodine for normal function, so it is particularly subjected to "endocrine disruptor" action. The human sodium/iodide symporter (hNIS) is an integral plasma membrane glycoprotein mediating the active transport of iodide into thyroid follicular cells, a crucial step for thyroid hormone biosynthesis. Beyond to perchlorate and thyocianate ions a few other inhibitors of iodide uptake have been described.


OBJECTIVE
The aim of this study was to investigate if 10 substances usually used as drugs in clinical practice were able to inhibit NIS-mediated iodide uptake in vitro.


METHODS
A CHO cell line stably expressing hNIS was used to test any inhibition of NIS-mediated iodide uptake exerted by drugs. Perchlorate and thyocianate ions were used as positive controls.


RESULTS
None of the analyzed substances was able to significantly inhibit iodide uptake in our system. As we expected, perchlorate and thyocianate ions were able to inhibit iodide uptake in a dose-dependent manner.


CONCLUSIONS
In conclusion, we carried out an in vitro assay to evaluate the potential inhibitory effect of common drugs on NISmediated iodide uptake by using CHO-hNIS cells. None of the analyzed substances was able to inhibit iodide uptake; only perchlorate and thyocianate were able to inhibit iodide uptake in a dose-dependent manner.
Agretti
P
P
Department of Endocrinology and Metabolism, Centro Eccellenza AmbiSEN, University of Pisa, Pisa, Italy.
Dimida
A
A
De Marco
G
G
Ferrarini
E
E
Rodrìguez Gonzàlez
J C
JC
Santini
F
F
Vitti
P
P
Pinchera
A
A
Tonacchera
M
M
D058888:14-alpha Demethylase Inhibitors / Q000737:chemistry / Q000494:pharmacology; D000666:Amphotericin B / Q000737:chemistry / Q000494:pharmacology; D000818:Animals; D018926:Anti-Allergic Agents / Q000737:chemistry / Q000494:pharmacology; D000890:Anti-Infective Agents / Q000737:chemistry / Q000494:pharmacology; D000893:Anti-Inflammatory Agents / Q000737:chemistry / Q000494:pharmacology; D001285:Atropine / Q000737:chemistry / Q000494:pharmacology; D001710:Biotin / Q000737:chemistry / Q000494:pharmacology; D002065:Buspirone / Q000737:chemistry / Q000494:pharmacology; D016466:CHO Cells / Q000187:drug effects / Q000378:metabolism*; D006224:Cricetinae; D003412:Cricetulus; D004464:Econazole / Q000737:chemistry / Q000494:pharmacology; D006801:Humans; D006854:Hydrocortisone / Q000737:chemistry / Q000494:pharmacology; D007454:Iodides / Q000378:metabolism*; D008795:Metronidazole / Q000737:chemistry / Q000494:pharmacology; D018727:Muscarinic Antagonists / Q000737:chemistry / Q000494:pharmacology; D010208:Papaverine / Q000737:chemistry / Q000494:pharmacology; D010472:Perchlorates / Q000494:pharmacology; D010726:Phosphodiesterase Inhibitors / Q000737:chemistry / Q000494:pharmacology; D011398:Promethazine / Q000737:chemistry / Q000494:pharmacology; D017366:Serotonin Receptor Agonists / Q000737:chemistry / Q000494:pharmacology; D013411:Sulfadiazine / Q000737:chemistry / Q000494:pharmacology; D027981:Symporters / Q000235:genetics / Q000378:metabolism*; D013861:Thiocyanates / Q000494:pharmacology; D013961:Thyroid Gland / Q000187:drug effects / Q000378:metabolism*; D000099209:Sodium-Iodide Symporters
D058888:14-alpha Demethylase Inhibitors; D000666:Amphotericin B; D018926:Anti-Allergic Agents; D000890:Anti-Infective Agents; D000893:Anti-Inflammatory Agents; D001285:Atropine; D001710:Biotin; D002065:Buspirone; D004464:Econazole; D006854:Hydrocortisone; D007454:Iodides; D008795:Metronidazole; D018727:Muscarinic Antagonists; D010208:Papaverine; D010472:Perchlorates; D010726:Phosphodiesterase Inhibitors; D011398:Promethazine; D017366:Serotonin Receptor Agonists; D013411:Sulfadiazine; D027981:Symporters; D013861:Thiocyanates; D000099209:Sodium-Iodide Symporters; C494474:perchlorate