Propylthiouracil

About: Propylthiouracil is a research topic. Over the lifetime, 2181 publications have been published within this topic receiving 46996 citations. The topic is also known as: Thyreostat® & 2,3-dihydro-6-propyl-2-thioxo-4(1H)-pyrimidinone.

The effects of iodides and other halides given with thiouracil.

Abstract: 1. Concurrent administration of iodide and thiouracil or propylthiouracil for two to six weeks results in thyroid glands which are 20 to 30 per cent lighter than those produced by the administration of thiouracil or propylthiouracil alone. 2. Iodide does not decrease the effectiveness of the goitrogenic drugs in lowering the metabolic rate. Consequently, its antigoitrogenic action cannot be attributed to an increase in the supply of available thyroid hormone. 3. The thyroid follicles of the rats receiving iodide with thiouracil contain more colloid and show less hyperplasia. The effect of the iodide seems to be best described as antithyrotropic in some sense.

Hepatic microsomal ethanol-oxidizing system (MEOS): increased activity following propylthiouracil administration.

Abstract: Treatment for 7 days with the thyreostatic drug propylthiouracil (5 mg/100 g of body weight) resulted in a hypothyroid hepatic state as shown by the marked decreased hepatic content of thyroxine and triiodothyronine. This regimen led to an enchanced activity of the microsomal ethanol-oxidizing system, whereas the activities of alcohol dehydrogenase and catalase remained unchanged. Moreover, a hyperthyroid hepatic state achieved following the daily administration of L-thyroxine (150 micrograms/100 g of body weight) or L-3,3', 5-triiodothyronine (10 micrograms/100 g body weight) for 7 days resulted in a similar increased activity of the microsomal ethanol-oxidizing system. Under these conditions, a decrease of alcohol dehydrogenase activity and an unaffected catalase activity was observed. These findings, therefore, show that the administration of either propylthiouracil or thyroid hormones results in an increased activity of the microsomal ethanol-oxidizing system, suggesting that the underlying mechanism for the induction of the microsomal ethanol-oxidizing system by propylthiouracil is independent of the action of thyroid hormones.

Type II thyroxine 5′-deiodinase in the rat thymus

Abstract: In the present study we have shown type II thyroxine 5'-deiodination (5'D) in the rat thymus. The enzyme activity was identified in crude extract homogenates by measuring the 125 I released from [3',5'- 125 I]thyroxine which is used as a substrate of the reaction. The release of 125 I is dependent on protein tissue concentration, time, temperature and pH, and is saturable by increasing the substrate concentration, indicating its enzymatic nature. Characteristics of the enzyme activity also include a low K m (9.1 nM), its dependence on dithiothreitol, and its inhibition by iopanoic acid, but not by propylthiouracil. Experiments to investigate the cellular location of the enzyme in the thymic gland showed that the enzyme is present in both stromal cells and thymocytes. At the subcellular level, 5'D activity was associated with cellular membranes. Thyroid status appears to regulate 5'D activity in rat thymus. Hypothyroidism caused an increase in thymus 5'D activity. The K m value remained unchanged (9.1 vs 10.5 nM) during hypothyroidism, but V max increased significantly from 17.7 fmol/mg protein per h in euthyroid rats to 53.5 fmol/mg protein per h in hypothyroid rats. 5'D activity was also modulated by catecholamines through β-adrenergic receptors because isoproterenol, but not methoxamine or clonidine, could activate the enzyme. Because these characteristics define the type II iodothyronine-deiodinating pathway in other tissues, we suggest that the rat thymus also shares this pathway.

Suppression of Thyroid Function by Pituitary Tumor MtTW5

Abstract: A transplantable pituitary tumor, MtTW5, which secretes prolactin and growth hormone but no TSH or ACTH, causes a marked increase in total body weight and in the weight of most internal organs. However, the pituitary glands of tumor-bearing rats weighed significantly less in proportion to body weight than did pituitaries in control rats. Incorporation of 131I into the trichloroacetic acid-soluble and the protein fractions of the thyroid and serum was measured. Less 131I was incorporated into these fractions of the thyroid and into the protein fraction of serum of tumor-bearing rats than in control rats. These results were obtained in intact female, spayed female, nephrectomized female and male rats. After acute treatment with propylthiouracil, tumor-bearing rats incorporated less 131I into their thyroids than did controls similarly treated with propylthiouracil. Thus, the primary defect in the thyroid of tumorbearing rats is in its inability to concentrate iodine from the blood. Histological examination o...