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Valinomycin-Induced Iodide Leakage without Impairment in Sodium-Dependent Iodide Transport in the Thyroid^*

KOSHI SAITO, KUNIHIRO YAMAMOTO, TAKAJI TAKAI and SHO YOSHIDA

Department of Endocrinology and Metabolism, Jichi Medical School Yakushiji 3311-1, Minamikawachi, Tochigi 329-04, Japan

Abstract

The mechanism of inhibition of I^– accumulation in the thyroid by valinomycin was investigated on a biological model. Phospholipid vesicles (P-vesicles) capable of Na⁺-dependent I^– accumulation were reconstituted with thyroid plasma membrane (PM). In P-vesicles internally loaded with K⁺, Na⁺- dependent I^– accumulation was observed in the presence of external Na⁺. The accumulated I^– was discharged from the vesicles by addition of valinomycin. In P-vesicles with internal choline⁺, Na⁺-dependent I^– accumulation also occurred, but I^– discharge was not induced by the addition of valinomycin. Pvesicles without a PM component readily accumulated I^– in the presence of both external K⁺ and valinomycin. P-vesicles with thyroid PM also accumulated I^– rapidly in the presence of external K⁺ upon the addition of valinomycin; however, the accumulated I was significantly discharged when the vesicles were loaded internally with Na⁺. A significant I^– discharge was not observed in the vesicles with or without thyroid PM when they were loaded with choline⁺ instead of Na⁺. Valinomycininduced I^– uptake without leakage was observed in both Na⁺- and choline⁺-loaded P-vesicles containing liver PM instead of thyroid PM.

These results indicate that valinomycin may inhibit I^– accumulation in thyroid cells according to the following mechanism: 1) valinomycin, a K⁺ carrier, induces K⁺ efflux to form a gradient of electrical potential with a negative charge within the cells, and 2) I^– is subsequently driven out down the gradient through the phospholipid bilayer. Na⁺-dependent I^– transport may not be impaired by valinomycin. (Endocrinology 113: 1031, 1983)

Footnotes

^* This study was supported in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, and Culture of Japan.

To whom requests for reprints should be addressed.

Present address: The Second Department of Internal Medicine, Chiba University School of Medicine, Chiba, Japan.

Received January 28, 1983.