Preservation of Sodium-Dependent Iodide Transport Activity By Methimazole and Mercaptoethanol in Phospholipid Vesicles Containing Thyroid Plasma Membranes: with Evidence of Difference in the Action of Perchlorate and Thiocyanate.

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Abstract
The effect of methimazole (MMI) and 2-mercaptoethanol (ME) on I- transport was studied using phospholipid vesicles (P-vesicles) made from porcine thyroid plasma membranes and soybean phospholipids by sonication. When buffer solutions contained either 1 mM MMI or 2 mM ME, I- uptake by P-vesicles in the presence of external Na+ was apparently higher than that in the absence of external Na+. Na+-dependent I+ uptake was inhibited by both ClO4- and SCN- added externally. When PM was treated with 4 mM N-ethylmaleimide prior to preparation of P-vesicles, the activity of Na+-dependent I+ transport was completely lost even when P-vesicles were incubated in the presence of ME. When neither MNI nor ME was added to buffers, I- uptake in the presence of external Na+ was not at all higher than that in the absence of external Na+. In these instances, however, I- uptake was much higher compared than the baseline uptake in the presence of MMI or ME, and was inhibited by external SCN- and not by ClO4- without relation to external Na+. These data indicate that MMI or ME has two distinct effects on our model system of I- transport. The one is preservation of the Na-dependent I- transport activity by protecting a sulfhydryl group, and the other is reduction of nonspecific I- binding to P-vesicles. In addition, ClO4- is a more specific inhibitor of thyroid I- transport than SCN-, when non-specific I- oxidation is imperfectly prevented.