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SUMMARY
The importance of the presence of iodine for the formation of iodoproteins larger than 19S thyroglobulin, i.e. 27S and larger iodoproteins (large-TG), was studied. Samples of colloid were collected in vivo by micropuncture of single rat thyroid follicles after treatment with a low iodine diet or potassium perchlorate. The protein composition of the colloid was analysed by microgel electrophoresis on polyacrylamide gels.
It was observed that the large-TG fractions were reduced by approximately 50% after treatment with a low iodine diet for 3 months. The large-TG fractions were almost absent after treatment with perchlorate for 3 weeks.
Administration of 5 or 10 μg potassium iodide to the animals on a low iodine diet resulted in a significant increase of the relative amount of the large-TG fractions in the colloid within approximately 2 h, the higher dose of KI producing a more pronounced accumulation of the large-TG fractions. Inhibition of protein synthesis by cycloheximide did not prevent the increase of large-TG proteins in animals on a low iodine diet after the administration of 5 μg KI. The administration of iodide to rats treated with potassium perchlorate did not result in the appearance of large-TG fractions.
It is concluded that the aggregation of thyroglobulin molecules occurs in the follicle lumen as a consequence of iodine administration. This formation of large-TG fractions does not require exocytosis of newly synthesized protein.
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Analysis of the protein composition of the thyroid colloid was performed in 28 patients operated on for hyperthyroidism. Fifteen of the patients were treated before the operation with carbimazole combined with thyroxine and 13 were treated with propranolol alone. Colloid was collected by micropuncture of single follicles in peroperative thyroid biopsies. The protein composition was analysed by microgel electrophoresis and densitometry, both in the colloid samples and in the supernatant fraction of homogenates of microbiopsies from the thyroid specimens.
The analyses showed that, during treatment with carbimazole and thyroxine, the relative amount of the larger thyroglobulin aggregates (S-TG) was decreased compared with the relative amount observed in the colloid from normal thyroid tissue. In the hyperfunctioning thyroid tissue from the propranolol-treated patients the protein composition of the colloid was similar to that observed in normal tissue and the relative amount of the S-TG fractions was significantly higher than in the carbimazole- and thyroxine-treated group.
It may be concluded that the increased release of thyroid hormones in hyperthyroidism is not combined with changes in the protein composition of the thyroid colloid. The decreased relative amount of the S-TG fractions in the thyroid colloid from patients treated with carbimazole and thyroxine was probably due to an insufficient capacity to iodinate thyroglobulin.
