DURING incubation in saline media containing sufficient 1-methyl-2-mercapto-imidazole (Tapazole ®) to inhibit organic iodinations, surviving thyroid slices accumulate inorganic iodide (1). An active transport has been implicated in this process and its physical optima have been defined (1). In the present experiments, the same preparation has been used to characterize further the biochemical phenomena which mediate the thyroidal transport of inorganic iodide. Thyroid slices have been suspended in serial dilutions of various metabolic inhibitors; the concurrent effects upon respiratory activity and the, accumulation of iodide have been measured. Recognizable difficulties are inherent in the use of metabolic inhibitors in cellular systems (2, 3). Most inhibitors have multifocal actions. Hence, activities in isolated enzyme preparations cannot be directly extrapolated to complex cellular phenomena. Furthermore, binding, degradation or volatilization of inhibitor may obscure quantitative relationships. Negative experimental results may merely reflect inadequate cellular penetration. These limitations are equally applicable to studies conducted with slices in vitro or with animals in vivo. The former technique, however, eliminates such variables as blood flow, concentration of inhibitor, systemic toxicity, and the indirect effects of extrathyroidal regulators (e.g., pituitary).
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Freinkel et al. (1955) studied this question.
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