Abstract
SummarySince ClO4- accelerated thyroidal 131I release in intact rats or in hypophysectomized rats treated with TSH, and since it failed to do so in T4-treated rats, it seemed that ClO4- interfered with the recycling of iodide derived from free iodotyrosines. Similarly, MTU did not increase the rate of release of 131I in T4-treated rats, but did significantly so in TSH-treated, hypophysectomized rats. It thus seemed that intrathyroidally recycling iodide was largely from free iodotyrosines produced by hydrolysis of thyroglobulin. ClO4- was similarly effective as MTU and PTU in TSH-treated hypophysectomized rats, but it was less effective in intact rats. This difference was due to the fact that more TSH was secreted in response to PTU or MTU in intact rats thus producing a large amount of iodotyrosines through the hydrolysis of thyroglobulin.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call