THYROTROPHIC HORMONE ACTIVITY IN HYPOPHYSECTOMIZED RATS EXPOSED TO COLD AND RECEIVING ASCORBIC ACID

1958 ◽  
Vol 36 (11) ◽  
pp. 1099-1104
Author(s):  
André DesMarais

Hypophysectomized rats were treated for 5 days with 0.05 unit of thyrotrophic hormone (TSH) daily, with or without administration of 150 mg of ascorbate per day, and either exposed to cold (14 °C) or kept at room temperature (24 °C). No effect of exposure to cold or ascorbate treatment could be observed on the thyroid–TSH relationship. Any effect of ascorbate treatment in these animals appears to be mediated through the circulating thyroid hormones.

1958 ◽  
Vol 36 (1) ◽  
pp. 1099-1104
Author(s):  
André DesMarais

Hypophysectomized rats were treated for 5 days with 0.05 unit of thyrotrophic hormone (TSH) daily, with or without administration of 150 mg of ascorbate per day, and either exposed to cold (14 °C) or kept at room temperature (24 °C). No effect of exposure to cold or ascorbate treatment could be observed on the thyroid–TSH relationship. Any effect of ascorbate treatment in these animals appears to be mediated through the circulating thyroid hormones.


1949 ◽  
Vol 27e (6) ◽  
pp. 349-363 ◽  
Author(s):  
M. Thérien ◽  
J. Leblanc ◽  
O. Héroux ◽  
L. P. Dugal

It has been shown recently by Dugal and Thérien that during a short or long exposure to cold, the normal hypertrophy of the adrenals is completely prevented by large doses of ascorbic acid, and that, nevertheless, at the same time, resistance is increased towards the same damaging agent. So, the most universally accepted criterion of damage caused by stress is abolished when the animals exposed to cold receive large doses of ascorbic acid. Starting from that observation, it was natural to wonder what would be the effects of the ascorbic acid on the biological changes normally associated with the hypertrophy of the adrenals during exposure to cold. The present paper describes the experimental studies made in that connection; the results obtained show that: (1) ascorbic acid (a) partly inhibits the thymus atrophy normally encountered upon exposure to any stress including cold, (b) accelerates in a very significant way the enlargement of the thyroid, (c) is responsible for an increase in weight of the spleen, whereas the control animals, on the contrary, show a decrease in weight of the same organ; (2) the histamine content of the adrenals, which increases at room temperature under the influence of ascorbic acid, is significantly decreased during exposure to cold under the influence of the same substance; (3) the activity of the adrenals, far from being inhibited by ascorbic acid is even increased if the cholesterol changes are taken as an index of that activity; (4) the initial hypotension—due to cold—found in our controls, is prevented by large doses of ascorbic acid; on the other hand, if hypertension develops after long exposure to cold, the subsequent administration of large doses of ascorbic acid restores the blood pressure to normal. Confirmation has also been obtained for the previously reported observation that ascorbic acid prevents the hypertrophy of the adrenals during exposure to cold.


1955 ◽  
Vol 33 (1) ◽  
pp. 677-680
Author(s):  
L.-P. Dugal ◽  
A. Desmarais ◽  
P. M. Gagnon

Modification of the response of the adrenal gland to ACTH was observed in hypophysectomized rats exposed to cold with or without ascorbic acid treatment. Changes in weight and metabolic activity of the gland were used to measure the adrenal response. All comparisons were made between the left and the right adrenal of each animal before and after treatment. The results obtained show that cold stress increases the response of the adrenal to a standard dose of two units of ACTH; they also indicate that ascorbic acid administration increases so much the responsiveness of the adrenal gland to ACTH at room temperature that such a response is not enhanced by exposure to cold.


1955 ◽  
Vol 33 (4) ◽  
pp. 677-680
Author(s):  
L.-P. Dugal ◽  
A. Desmarais ◽  
P. M. Gagnon

Modification of the response of the adrenal gland to ACTH was observed in hypophysectomized rats exposed to cold with or without ascorbic acid treatment. Changes in weight and metabolic activity of the gland were used to measure the adrenal response. All comparisons were made between the left and the right adrenal of each animal before and after treatment. The results obtained show that cold stress increases the response of the adrenal to a standard dose of two units of ACTH; they also indicate that ascorbic acid administration increases so much the responsiveness of the adrenal gland to ACTH at room temperature that such a response is not enhanced by exposure to cold.


1961 ◽  
Vol 36 (1) ◽  
pp. 73-82 ◽  
Author(s):  
Darrell N. Ward ◽  
Mabelle Adams-Mayne ◽  
Jane Wade

ABSTRACT A fraction possessing luteinizing hormone activity isolated by chromatography on a carboxymethyl cellulose ion exchange column and previously designated LH1 has been studied. The potency of this fraction relative to a reference standard was less when assayed by the ovarian ascorbic acid depletion method than previously obtained with the ventral prostate assay in hypophysectomized rats. It has been found that the LH1 fraction possesses heterogeneity upon sedimentation in the ultracentrifuge directly after chromatography, thus does not dissociate into other molecules with luteinizing activity with subsequent handling as previous evidence had suggested. The LH1 fraction was shown to arise from association of luteinizing activity with an acidic »combining« protein from the original sheep pituitary glands. Thus the LH1 fraction was a chromatographic artefact and presumably has no physiological significance. The »combinig« protein was analyzed for its amino acid composition to demonstrate the acidic nature of this material.


1961 ◽  
Vol 37 (2) ◽  
pp. 176-182 ◽  
Author(s):  
Elliott J. Collins ◽  
Vernon F. Baker

ABSTRACT The characteristics and nature of the effect of growth hormone on the incorporation of radio-sulfate into the costal cartilage of hypophysectomized rats has been studied. The time-response studies indicate that a reliable estimation of growth hormone activity can be ascertained within a 24 hour period, and a reproducible dose-related response can be obtained at dosage levels ranging from 12-48 μg. Growth hormone stimulates the synthesis of organic sulfates and accumulation of inorganic sulfates within 48 hours.


1962 ◽  
Vol 39 (4) ◽  
pp. 527-538 ◽  
Author(s):  
Pavo Hedner ◽  
Claus Rerup

ABSTRACT Measurements of plasma corticosteroid levels and adrenal ascorbic acid concentration in steroid blocked and hypophysectomized rats were performed. It was found that prednisolone and dexamethasone were effective in blocking endogenous corticotrophin release within 3–4 hours after subcutaneous injection. These agents also prevented completely the normally occurring rise in plasma corticoid levels after exposure of the rats to ether. Abdominal surgery (unilateral adrenalectomy) resulted in a slight but significant rise in plasma corticoid levels in spite of dexamethasone blockade. The values of adrenal ascorbic acid were not affected significantly. The blocking effect of two daily subcutaneous injections of a high dose of dexamethasone persisted for about one week after the last injection. The sensitivity of the plasma corticoid response was essentially the same in hypophysectomized and dexamethasone blocked rats. The lower part of the log dose response curve was found to be clearly non-linear in the plasma corticoid method following intravenous corticotrophin injection. As a consequence the dose level in quantitative assays of intravenously injected corticotrophin are, in our hands, of the same order as in the adrenal ascorbic acid depletion method.


2008 ◽  
Vol 233 (10) ◽  
pp. 1309-1314 ◽  
Author(s):  
A. V. Capuco ◽  
E. E. Connor ◽  
D. L. Wood

Thyroid hormones are galactopoietic and help to establish the mammary gland’s metabolic priority during lactation. Expression patterns for genes that can alter tissue sensitivity to thyroid hormones and thyroid hormone activity were evaluated in the mammary gland and liver of cows at 53, 35, 20, and 7 days before expected parturition, and 14 and 90 days into the subsequent lactation. Transcript abundance for the three isoforms of iodothyronine deiodinase, type I ( DIO1), type II ( DIO2) and type III ( DIO3), thyroid hormone receptors alpha1 ( TRα 1), alpha2 ( TRα 2) and beta1 ( TRβ 1), and retinoic acid receptors alpha ( RXRα) and gamma ( RXRγ), which act as coregulators of thyroid hormone receptor action, were evaluated by quantitative RT-PCR. The DIO3 is a 5-deiodinase that produces inactive iodothyronine metabolites, whereas DIO1 and DIO2 generate the active thyroid hormone, triiodothyronine, from the relatively inactive precursor, thyroxine. Low copy numbers of DIO3 transcripts were present in mammary gland and liver. DIO2 was the predominant isoform expressed in mammary gland and DIO1 was the predominant isoform expressed in liver. Quantity of DIO1 mRNA in liver tissues did not differ with physiological state, but tended to be lowest during lactation. Quantity of DIO2 mRNA in mammary gland increased during lactation ( P < 0.05), with copy numbers at 90 days of lactation 6-fold greater than at 35 and 20 days prepartum. When ratios of DIO2/DIO3 mRNA were evaluated, the increase was more pronounced (>100-fold). Quantity of TRβ 1 mRNA in mammary gland increased with onset of lactation, whereas TRα 1 and TRα 2 transcripts did not vary with physiological state. Conversely, quantity of RXRα mRNA decreased during late gestation to low levels during early lactation. Data suggest that increased expression of mammary TRβ 1 and DIO2, and decreased RXRα, provide a mechanism to increase thyroid hormone activity within the mammary gland during lactation.


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