Propylthiouracil inhibits the conversion of <sc>l</sc>-thyroxine to <sc>l</sc>-triiodothyronine: <i>An explanation of the antithyroxine effect of propylthiouracil and evidence supporting the concept that triiodothyronine is the active thyroid hormone</i>

Jack H. Oppenheimer; Harold L. Schwartz; Martin I. Surks

doi:10.1172/JCI107063

¹Endocrine Research Laboratory, Department of Medicine, Montefiore Hospital and Medical Center and the Albert Einstein College of Medicine, Bronx, New York 10467

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¹Endocrine Research Laboratory, Department of Medicine, Montefiore Hospital and Medical Center and the Albert Einstein College of Medicine, Bronx, New York 10467

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¹Endocrine Research Laboratory, Department of Medicine, Montefiore Hospital and Medical Center and the Albert Einstein College of Medicine, Bronx, New York 10467

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Published in Volume 51, Issue 9 on September 1, 1972
J Clin Invest. 1972;51(9):2493–2497. https://doi.org/10.1172/JCI107063.
© 1972 The American Society for Clinical Investigation

Published September 1, 1972 - Version history

6-n-propylthiouracil (PTU) administered to male Sprague-Dawley rats maintained on 2 and 5 μg L-thyroxine (T₄)/100 g body weight resulted in a marked reduction in the rate of conversion of L-thyroxine to L-triiodothyronine (T₃). These effects could not be ascribed to induced hypothyroidism since the group maintained on 5 μg T₄/day had normal levels of liver mitochondrial alpha glycerophosphate dehydrogenase. In confirmation of previous studies, PTU also reduced the fractional rate of deiodination of T₃. These observations provide a possible explanation of the many published observations indicating that PTU antagonizes the tissue effects of T₄ but not of T₃. The data suggest that monodeiodination of T₄ but not of T₃ is essential before hormonal effects can be manifested at the cellular level.