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Transport of free 211At and 125I- in thyroid epithelial cells: effects of anion channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid on apical efflux and cellular retention.

Journal article
Authors Ulrika Lindencrona
Eva Forssell-Aronsson
Mikael Nilsson
Published in Nuclear medicine and biology
Volume 34
Issue 5
Pages 523-30
ISSN 0969-8051
Publication year 2007
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Institute of Clinical Sciences
Pages 523-30
Language en
Links dx.doi.org/10.1016/j.nucmedbio.2007...
Keywords 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid, administration & dosage, Animals, Antiporters, antagonists & inhibitors, Astatine, pharmacokinetics, Biological Transport, Active, drug effects, physiology, Cells, Cultured, Dose-Response Relationship, Drug, Epithelial Cells, drug effects, metabolism, Iodine Radioisotopes, pharmacokinetics, Metabolic Clearance Rate, drug effects, Radiopharmaceuticals, pharmacokinetics, Swine, Symporters, antagonists & inhibitors, Thyroid Gland, cytology, drug effects, metabolism
Subject categories Physiology, Radiological physics

Abstract

INTRODUCTION: Astatine ((211)At; alpha-emitter; t(1/2)=7.21 h) shares several features with its halogen neighbour iodine. In the present study, we investigated whether 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) can be used to increase the cellular retention time of (211)At and radioiodide in thyroid epithelial cells. METHODS: The transepithelial transport and cellular uptake of (211)At and (125)I(-) were studied simultaneously in porcine thyrocytes cultured in bicameral chambers. The cells were prestimulated with thyroid-stimulating hormone (TSH) or epidermal growth factor (EGF) for 48 h. In addition, the acute effects of DIDS and forskolin were investigated. RESULTS: The transepithelial transport of both radionuclides was stimulated by TSH and down-regulated by EGF. DIDS rapidly reduced the efflux and increased the cellular content of (125)I(-) in control and TSH-stimulated cells, whereas DIDS had no effect on (125)I(-) transport in EGF-treated cells. DIDS blocked the (211)At efflux only in TSH-stimulated cells. Unexpectedly, DIDS caused an accelerated efflux of (211)At in both control and EGF-stimulated cells and, furthermore, reduced the cellular content of (211)At in the EGF-stimulated cultures. DIDS had no effect on the forskolin-induced efflux of the two radionuclides. CONCLUSIONS: The magnitude of thyroidal (211)At uptake and efflux is similar to that of (125)I(-), strongly dependent on the functional activity of the cells. However, (211)At efflux likely involves several permeating mechanisms with different sensitivity to DIDS, which are at least partly not shared by (125)I(-). The results suggest that anion channel blockage is potentially useful to increase the absorbed dose from both (211)At and radioiodine in NIS-expressing tumours.

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