Abstract
The mechanism by which salicylate depresses thyroid function has been investigated in normal rats. Bio-assay of TSH in the plasma of rats was carried out using a modification of the McKenzie mouse procedure. It was demonstrated that the administration of salicylate, 2,4-dinitrophenol and γ-resorcylate (2,6-dihydroxybenzoate) significantly depressed circulating TSH in association with a significant depression in plasma PBI. There was no effect of p-hydroxybenzoate on plasma TSH or plasma PBI. Previous suggestions that the hypermetabolism induced by salicylate and 2,4-dinitrophenol was responsible for the depression in thyroid function may now be excluded, since γ-resorcylate lacks this effect. Using the dialysis procedure of Christensen for the determination of free thyroxine, it has been demonstrated that the in vitro addition of salicylate and γ-resorcylate to rat serum increased the rate of dialysis of radiothyroxine; p-hydroxybenzoate produced a smaller effect. Circulating free thyroxine was elevated a...
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