EFFECT OF 2,4-DINITROPHENOL ON THYROID FUNCTION IN MAN*

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Abstract
Diniteophenol has long been recognized as an agent capable of inducing hypermetabolism in various animal species by virtue of its uncoupling effect on oxidative phosphorylation within the Krebs tricarboxylic acid cycle (1, 2, 3). Thompson and associates (4) demonstrated a calorigenic effect of dinitrophenol in man, even when the subject was hypothyroid. In 1950 Wolff first described lowering of the serum proteinbound iodine (PBI) level in rats made hypermetabolic with 2,4-dinitrophenol (5). Radioactive iodine (I131) studies failed to show inhibition of thyroidal iodine uptake or organification. Histologically, the pituitary and thyroid were also found to be normal following administration of 2,4-dinitrophenol (6). Goldberg et at. recently reported studies in rats which were interpreted as showing: a) decreased 24-hour thyroidal uptake of I131, b) decreased rate of iodine organification, and c) increased disappearancerate of serum protein-bound iodine131 (PBI131) from the circulation following administration of dinitrophenol (7). In vitro studies with sheep thyroid slices have shown that iodide transport across cell membranes can be inhibited by 2,4-dinitrophenol in concentrations adequate to reduce oxygen uptake (8).