EFFECTS OF PROPYLTHIOURACIL (PTU) ADMINISTRATION ON THE SYNTHESIS ANDSECRETION OF THYROGLOBULIN IN THE RAT-THYROID GLAND - A QUANTITATIVE IMMUNOELECTRON MICROSCOPIC STUDY USING IMMUNOGOLD TECHNIQUE

To clarify the effects of an antithyroid drug on the kinetics of thyro globulin synthesis, secretion, and reabsorption in the thyroid follicl es, propylthiouracil (PTU) was administered to rats and the thyroid gl ands were examined by a refined post-embedding immunogold technique du ring and after withdrawal of PTU. Seven-wk-old male Wistar rats were a dministered with 5 mg of PTU/d through a gastric tube, and sacrificed at 1 and 2 wk of administration and at 1, 2, and 3 d, and 1, 2, 3, and 4 wk, after discontinuation. The administration of PTU caused a remar kable dilatation of the rER and Golgi apparatus, but these areas gradu ally recovered after withdrawal of PTU. During the experiment, no sign ificant change in the density of thyroglobulin (Tg) was observed excep t for a transient increase immediately after withdrawal of PTU. The ex pression of Tg on subapical vesicles (SV) and follicular colloid took a relatively parallel course; Increasing during administration of PTU and decreasing with a transient peak immediately after treatment was d iscontinued. In contrast to the remarkable changes in the morphology o f compartments involved in Tg synthesis, the development of colloid dr oplets and formation of secondary lysosomes were suppressed during and after discontinuing administration of PTU. However, the basic pattern of the gradient of Tg density among the cellular compartments was ess entially retained in the experimental group. Thus the present immunoel ectron-microscopic study provided evidence that administration of PTU stimulates the synthesis and secretion of Tg in the follicular epithel ium in vivo, and, also, suppresses reabsorption and degradation of Tg. Further, it was speculated that the density gradient of Tg among the compartments involved in Tg synthesis, secretion and storage is regula ted by an unknown constitutive mechanism and not by the thyroid-stimul ating hormone (TSH)-TSH receptor-mediated system.