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J B Rognoni

Publications and source records attributed to J B Rognoni.

31 records · Page 2Linked to original sources

Negative effect of iodide on the survival of newly divided epithelial cells in chronically stimulated rat thyroid.

The aim of this work was to investigate some aspects of the thyroid epithelial cell kinetics during the iodide-induced involution of a hyperplastic goitre in the rat. Rats were made iodine-deficient for 6 months, and propylthiouracil (PTU) (0.15%) was added to the diet during the last 2 months. Thereafter, rats were refed with iodide and PTU was removed (day 0). Forty-eight hours previously, all the rats were injected with tritiated thymidine ([3H]TdR) (1 microCi/g). Some animals were killed 1 hr or 24 hr after [3H]TdR injection (i.e. on day -2 and -1, day 0 corresponding to the restoration of a normal iodine diet); the other animals were killed after different delay periods and following [3H]TdR injection. Autoradiography of thyroid sections, iodine determination of plasma iodide and protein-bound iodine (PBI), and RIA of plasma thyroid stimulatory hormone (TSH) were performed. Plasma TSH concentration was very high on day 0 of iodide refeeding (3000 +/- 330 ng/ml) and remained at this level until day 8. Plasma PBI was very low on day 0, remained so until day 4 and greatly increased on day 8. Plasma iodide was also very low on day 0, but markedly increased on day 1, then did not vary significantly until day 43 of iodine refeeding. Thyroid weight, elevated on day 0, decreased relatively quickly until day 30, then more slowly until day 73. The [3H]TdR labelling index (LI) of the thyroid epithelial cells (TEC) was high on day 0 (56 +/- 3 labelled cells/10,000 cells), and 24 hr thereafter increased to 104 +/- 3, by division of the labelled cells. On day 1 of iodine refeeding, the LI had abruptly decreased to about half this value and then remained stable for 3 more days. Between day 4 and day 16, a progressive decline in the LI, (by about 3-4 per day), was observed. The LI showed no further modification, up to day 73, the longest period investigated. The decrease in LI occurred without any significant changes in the labelling intensity (grain count) of the remaining labelled cells between day 1 and 16, this indicates that no cell division took place during this period. The data are therefore interpreted as showing a biphasic elimination after iodide refeeding, of cells that were actively proliferating during the goitrous state.(ABSTRACT TRUNCATED AT 400 WORDS)

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Iodide accumulation into thyroid Golgi vesicles.

Pig thyroid Golgi vesicles incubated in a suitable medium were able to concentrate iodide from the medium. This trapping required the integrity of the vesicles, was time- and temperature-dependent, and was inhibited by a competitive inhibitor of iodide active transport (perchlorate), suggesting a facilitated transport mechanism.

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[Effect of cycloheximide on nuclear triiodothyronine receptors in the pituitary of the normal and hypothyroid rat].

Cycloheximide (Cy), an inhibitor of protein synthesis was found to provoke a dose-dependent decrease of the hypophysis T3 nuclear receptors (T3nR) concentration in normal rats. In thyroidectomized rats, the reduced T3nR density was found to be normalized within 3 hrs. after a single injection of T3. Pretreatment with Cy inhibited the T3 effect on its own receptors, whereas Cy given after T3 was partially or not effective. These data suggest that the half-life of T3nR in the hypophysis is short (about 3 hrs.), and that it depends on protein neosynthesis.

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[Possible regulation of the growth of thyroid tissue by plasma iodide].

Rats on iodine deficient diet for 6 months received propylthiouracil (PTU) (0.15%) during the last 2 months. At the end of this treatment, PTU was withdrawn and the rats were iodine refed. 48 hrs. before the iodine refeeding all rats were injected with 3H thymidine. The results showed that some prelabelled cells in the hyperplastic goitre preferentially disappeared during its involution and therefore are more sensitive to iodine.

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Thyroid morphological and functional heterogeneity: impact on iodine secretion.

Thyroid iodine turnover heterogeneity includes morphological (cellular and colloidal distribution space for iodide) and functional heterogeneity (hormone synthesis in the colloid). In 'normal' rats, both iodide actively trapped by the epithelial cell and that coming from deiodination of iodotyrosines present the same probability for thyroglobulin (Tg) iodination (Tg iodination flux: 4.0 +/- 0.3 micrograms I/day). A portion of the thyroid iodide is sequestered in the colloid lumen and is inoperative in the Tg iodination mechanisms. The masses of cell and colloid compartments are equivalent (0.018 +/- 0.002 micrograms I) while colloid iodide concentration is twice that of the cell (0.11 and 0.06, respectively). The turnover of about 3 micrograms I of colloid iodine (Tg) is follicle diameter-dependent (inter-follicular heterogeneity) and it is mainly characterized by 2 different half lives of 8 and 16 hours, respectively. Ninety percent of the thyroid iodine (hormone) secretion (1.10 +/- 0.11 micrograms I/day) is provided by this compartment rich in iodotyrosine residues (70%). The remaining 10% of iodine secretion is provided by a Tg pool (7 micrograms I) characterized by 2 compartments (intra-follicular heterogeneity) with slow and very slow turnovers. The longer the transit time of Tg molecules in the colloid, the higher their iodothyronine content.

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Respective roles of circulating T4 and T3 in control of TSH secretion in severely iodide-deficient rats.

After a 6-month iodide deficiency, Wistar male rats were submitted to a normal iodine diet (20 and 50 micrograms of 127I daily). Plasma T3, T4 and TSH were determined by RIA from 0 to 140 days of iodide refeeding. A highly significant correlation was found between plasma TSH and T4 concentrations, but not between plasma TSH and T3 levels. These data suggest that an increase in plasma T3 alone, up to the normal value, is not able to inhibit TSH secretion. It is only when a certain plasma T4 concentration is also reached, resulting in further T3 formation through deiodination, that TSH secretion is inhibited.

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Vascularization and iodide transport down regulation in rat goitre.

This study was designed to investigate, in the rat, the regulation of the amount of thyroid iodide and of its organification during the involution of an experimentally induced goitre. The goitre was obtained by drastic iodine deficiency; male Wistar rats received an iodide deficient diet for 6 months, supplemented with PTU during the last 2 months. The study was followed for 16 days after the beginning of iodide refeeding (daily iodine intake = 50 micrograms). The thyroid iodide, total thyroid organic iodine and plasma iodide, PBI and TSH concentrations were determined from day 0 to 16 and compared to their control values (rats on a normal iodide diet for 6 months). In addition, a stereological study was carried out to determine if the extent of the gland vasculature might be implicated in the regulation of the thyroid iodide content. The plasma TSH concentration was very high and constant for 8 days (2.40 +/- 0.37 and 2.45 +/- 0.43 on day 0 and 8 respectively vs 0.25 +/- 0.12 microgram/ml in control rats), whereas iodination and secretion were blocked for 4 days (0.34 +/- 0.19 and 0.5 +/- 0.1 on day 0 and 4 respectively vs 14.4 +/- 2.0 micrograms 127I/gland in control rats) (Wolff-Chaikoff effect). Thyroid iodide amount increased enormously for 2 days (2.5 +/- 0.6 and 2.45 +/- 0.55 respectively on day 1 and 2 vs 0.09 +/- 0.01 micrograms 127I/gland on day 0), then strongly decreased between 2 and 4 days (1.15 +/- 0.27 127I/gland).(ABSTRACT TRUNCATED AT 250 WORDS)

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[Retroinhibition of thyroid iodide active transport in rats, after a long iodine deficient diet followed by a normal iodine diet].

Rats were submitted to an iodine deficient diet during 6 months. At the end of this treatment, normal iodine diet was given to the animals during 16 days. For the first two days of iodine refeeding, thyroidal iodide was strongly stored, which is explained by a very stimulated iodide pump and by an iodination blockade. After this latency, the thyroidal iodide promptly decreased whereas iodide pump was always activated, and iodination still inhibited. A retroinhibition by thyroidal iodide on its active transport is postulated.

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Correlation between thyroid-follicle fusion and structural modifications of the epithelial cells. A quantitative study in the adult rat.

Changes in thyroid structure induced by a decrease in TSH or iodide-dependent stimulation were quantified by stereological analysis of light micrographs. Studies were carried out on intact (R5) and hypophysectomized (R5H) rats receiving 5 micrograms iodide, and on intact rats (R5O) receiving 50 micrograms iodide daily. For R5H- and R5O-thyroids, the mean parameters of the epithelial cells, height, volume and lateral membrane area, were smaller than those of R5-thyroids. An inverse shift was observed for the apical membrane area, whereas the peripheral membrane area was unchanged. The number of epithelial cells was similar in each of the three groups; however, the number of follicles was greater in R5-thyroids, suggesting that follicular fusion occurs in R5O- and R5H-thyroids. This was confirmed by direct observation. The present results demonstrate that in adult rats a lack of TSH or an increased iodide diet (insufficient to produce a physiopathological state) induce follicle fusion probably by means of cellular reorganization. This increase in follicle size could be involved in the regulation of thyroid iodine turnover.

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Age-dependent sensitivity of basal cells in mouse vaginal epithelium towards the diferentiating action of estrogen.

Following ovariectomy, the vaginal epithelium of the mouse is reduced to two layers of cells, the basal layer that constitutes the germinative compartment and surface layer. Under estrogenic influence, this tissue undergoes keratinization at the expense of asal cell only. The initially superficial cells are progressively sloughed, without taking part in the cornification process. We have shown previously that within the first 12 hours after estrogen administration (that is, before any change in mitotic activity is detected) an intermediate layer of cells is formed. Thurs, a migratory process is induced, which leads to a very rapid redistribution to basal cells into two layers...

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