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Abstract: The role of protein synthesis in iodide-induced suppression of subsequent iodide transport (iodide autoregulation) was studied in cat thyroid slices. Thyroid slices were pretreated for 60-120 min in the presence or absence of either excess (30 microM) sodium iodide, inhibitors of protein synthesis, or both. Tissue was then washed in the presence of 2 mM methimazole to prevent subsequent iodination reaction and remove excess iodide. Iodide transport activity was finally evaluated by measurement of the ratio of tissue to medium iodide concentrations in 90-min incubations. Addition of 0.1 mM cycloheximide during the preexposure of thyroid tissue to excess iodide had no effect on either control levels of iodide transport or iodide-induced autoregulation. However, if thyroid tissue was treated with cycloheximide alone for 1 h before preexposure to excess iodide, there was a significant reduction in the degree of iodide-induced induced autoregulation. Similar results were obtained with pretreatment of the tissue with 0.5 mM puromycin and 1 microgram/ml emetine. These findings suggest that protein synthesis is involved in the mechanism of thyroid autoregulation of iodide transport. Cycloheximide had no effect on the ability of excess iodide to reduce TSH-stimulated cAMP formation. Two-dimensional gel electrophoresis-isoelectric focusing and Sephadex G-25 column chromatography employing dual-isotope comparison of iodoprotein labeling of control and cycloheximide-treated tissue suggest that the ability of cycloheximide to suppress iodide-induced autoregulation is associated with the reduced iodination of an 8- to 10-kilodalton soluble component of the thyroid gland.
Autoregulation of thyroid iodide transport: evidence for the mediation of protein synthesis in iodide-induced suppression of iodide transport.