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Department of Physiology and Biophysics, University of Tennessee Center for the Health Sciences Memphis, Tennessee 38163
Address requests for reprints to: Dr. L. Van Middlesworth, Department of Physiology and Biophysics, University of Tennessee, 894 Union Avenue (NA 426), Memphis, Tennessee 38163.
Abstract
Mice were depleted of iodine and fed a 125I-labeled low iodine diet. After they developed isotopic equilibrium they were given T-2 mycotoxin, in doses 34% to. 14% of LD50/day for 4 to 12 days. In all cases T-2 toxin caused loss of thyroid iodine from which the animals recovered when the T-2 toxin was stopped. When iodine intake was adequate, the T-2 toxin had no statistically significant effect on the thyroid iodine content. Since T-2 toxin is known to block the initiation of some protein synthesis, it may block thyroglobulin synthesis, and, in stimulated thyroids, limited hydrolysis may continue. Therefore, when the thyroids were stimulated and thyroglobulin was depleted, a blockade of thyroglobulin synthesis may have caused further depletion of thyroidal iodine. (Endocrinology 118: 583–586, 1986)
Footnotes
* This investigation was partly supported by Research Career Award 4K06-AM-00040-2 from the NIH, by Research Contract DE-AS05-76EV1643 from the U.S. Department of Energy, and Grant BRSGRR05423 from the University of Tennessee.
Received October 2, 1985.
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