Abstract
Attention has been called as one of the major therapeutical problems to the recent increase of hypothyroidism which develops as a sequela after treating hyperthyroidism with radioactive iodine. However, the mechanism of its developement is as yet poorly understood.
As a means to elucidate this mechanism, biosynthetic changes in the amount of in-trathyroidal iodoamino acids and variations of 131I uptake after administration of 131I were studied in rats and discussed.
Male rats of Wistar strain were divided into 7 groups (groups A-G) . Fifty μci of 131I were given intraperitoneally to group A and 200 μci of 131I to group B, C and D. After 24 hours of 131I administration, 0.1 mg of methyl-mercaptoimidazole (MMI) was given daily to group C and 100 μg of potassium iodide (KI) was given daily to group D for 6 days. Group E and F were given only MMI and KI respectively and served as the control to groups C and D. Nothing was administered to group G which served as the normal control. Four hour-131I uptake was determined and intrathyroidal iodoamino acids were analysed paper-chromatogra-phically for periods from 4 hours up to 60 days after the administration of 131I. In the animals treated with 50 μci of 131I, 4 hr-131I uptake and thyroid hormone biosynthesis increased transiently 24 hrs after, then remained within normal range. However, disturbances in organification of iodine and in MIT synthesis continued for further experimental period.
In the animals treated with 200μci of 131I, strong disturbances in iodine uptake was observed in the early stage, whereas the biosynthesis of intrathyroidal iodomaino acids were disturbed in all stages. As compared to the other processes, disturbance in iodine accumulation and in MIT synthesis was found slight. Animals given either MMI or KI after 131I administration showed less disturbance in iodine uptake in early stage than in those adminster-ed 131I alone, although in later stage, the iodine uptake decreased in similar way to those administered 131I alone.
Biosynthesis of intrathyroidal iodoamino acids in these animals remained normal for a relatively longer period as compared with the animals given 131I alone. Prevention of radiation hazards, however, cannot be expected by as much dose of MMI or KI as this, since organization of iodine becomes intensely disturbed sooner or later.
It is apparent from these data that administration of 131I in large dose gives rise to strong dysfunction of the thyroid with no evident recovery, while in relatively small dose, iodine uptake is transiently stimulated, then disturbed, but returns to the normal level, and biosynthesis of intrathyroidal iodoamino acids remains normal for a long period. However, a possibility still exists in latter case that eventual biosynthetic disturbance of iodoamino acids leads to hypofunction of thyroid.
