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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.


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Journal ArticleDOI
TL;DR: Data implicate both activation of the enzymes as well as increased amounts of types I and II protein kinase activity in the thyroid in response to goitrogen-induced hypertrophy and hyperplasia.

13 citations

Journal ArticleDOI
TL;DR: Variations in renin- angiotensin-aldosterone system (RAAS) in experimentally induced hyperthyroidism were studied and the active hormone is seen to be triiodothyronine, confirmed by using the antithyroid preparation, propylthiouracil, to inhibit the conversion of thyroxine.
Abstract: Variations in renin- angiotensin-aldosterone system (RAAS) in experimentally induced hyperthyroidism were studied. The changes observed in the RAAS in these conditions, evaluated through the plasma renin activity (PRA), are parallel to serum aldosterone concentration (AC). An increase in PRA and AC is produced following the administration of triiodothyronine, possibly through elevated adrenergic activity: beta-blocker, propranolol, returned the PRA and AC to normal. The active hormone is seen to be triiodothyronine, confirmed by using the antithyroid preparation, propylthiouracil, to inhibit the conversion of thyroxine. Propylthiouracil administration to hyperthyroid animals lowers the PRA and AC.

13 citations

Journal ArticleDOI
TL;DR: The block of organic iodine formation by excess iodide was reinvestigated, paying particular attention to the intrathyroidal iodide concentration, to the role of TSH and to changes in physicochemical properties of thyroglobulin.
Abstract: The block of organic iodine formation by excess iodide was reinvestigated, paying particular attention to the intrathyroidal iodide concentration, to the role of TSH and to changes in physicochemical properties of thyroglobulin. Maximal TSH stimulation was obtained by pretreating rats for 4 weeks with propylthiouracil followed by 2 days of a low-iodine diet. Three mg iodide was then injected every 12 hr and the thyroid glands were analyzed at daily intervals. The initially very high intrathyroidal iodide concentration decreased rapidly during the first 4 days of excess iodide, irrespective of whether TSH was high or suppressed by thyroxine injections. Thus TSH played only a minor part in the adaptation of the active iodide transport mechanism. Organic iodine formation was blocked during the first 4 days of iodide treatment. As soon as the intrathyroidal iodide fell below 0.1 μg per mg tissue, organic iodination resumed in TSH-stimulated glands. In animals with low TSH the escape from the block was delayed...

13 citations

Journal ArticleDOI
TL;DR: Administration of alcohol to rats through drinking water for 8 weeks produced a significant decrease in the liver vitamin A stores without causing any change in the plasma vitamin A levels.
Abstract: Administration of alcohol to rats through drinking water for 8 weeks produced a significant decrease in the liver vitamin A stores without causing any change in the plasma vitamin A levels. Treatment of the alcoholic rats with propylthiouracil for 2 weeks restored the liver vitamin A reserves to control levels.

13 citations

Journal ArticleDOI
TL;DR: The results clearly indicate that the growing heart has a marked ability to be rehabilitated from severe hypothyroid retardation, showing within 2 mo full compensation of cell number and nearly complete Compensation of cell growth.
Abstract: Measurement of total DNA, RNA, and protein as well as weight of the heart in male rats at 10, 25, 50, and 90 postnatal days revealed that hypothyroidism, as induced by administration from birth of the goitrogen propylthiouracil (PTU), results in highly significant reductions in cardiac cell proliferation and cell growth. These inhibitory effects on hyperplastic and hypertrophic growths were less drastic during the suckling period than during the postweaning period. In the latter period, heart growth of the hypothyroid animals was found to remain at a standstill with regard to all the parameters measured. When, after 25 days of hypothyroidism, PTU treatment was discontinued, the retarded heart showed marked signs of rehabilitation and compensatory development. Indeed, by day 90, total DNA content had essentially compensated for its deficit but total RNA, protein content, and weight, though showing marked compensatory surges (from 80-90% deficit to 20-30%), were not yet fully compensated. The results clearly indicate that the growing heart has a marked ability to be rehabilitated from severe hypothyroid retardation, showing within 2 mo full compensation of cell number and nearly complete compensation of cell growth. It is suggested that rehabilitation of the heart is brought about by physiological restoration not only of the thyroid hormones but also of growth hormone and possibly other thyroid-dependent growth factors.

13 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202342
202276
202138
202032
201934
201829