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  • Author: F Escobar del Rey x
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J. Bernal and F. Escobar del Rey

ABSTRACT

Thyroidectomized rats have been injected daily with 125I labelled L-thyroxine (T4*) and, once isotopic equilibrium was attained, divided into cold-exposed (4–10°C) and control (21–24°C) groups, the daily T4* administration being continued till the end of the experiment. Fourteen days after onset of cold exposure, the total I* of different organs and of the carcass was determined and the tissues submitted to extraction and paper chromatography for the separation of T4 and T4-derived I-containing compounds. The activity of intramitochondrial α-glycerophosphate dehydrogenase (α-GPD) was measured in kidneys and liver. It was found that the total amount of I* was intensely decreased in all samples from cold-exposed animals. The proportion of this I* which was non-extractable was the same, in all tissues, for cold-exposed and control rats. The % of extractable tissue radioactivity in the form of T4 was decreased, and that found as T4-derived T3 was increased, in all samples from cold-exposed animals.

The T3/T4 ratio was increased more than two-fold in all tissues studied. The concentration of T4 decreased significantly in all tissues, whereas the concentration of T3 in tissues of cold-exposed rats did not decrease. It actually increased in kidneys and lungs, and remained the same in liver and carcass. Despite the decrease in the concentration of T4 in the kidneys, α-GPD activity was increased in this tissue, where the concentration of T3 was increased. No change in the α-GPD activity was found for the liver, where the concentration of T3 was the same for cold-exposed and control rats.

Thus, it appears likely that the conversion of T4 to T3 is increased by the exposure to cold of thyroidectomized rats on a constant dose of T4. α-GPD activity in a given tissue appears to be more closely related to the concentration of T3, than to that of T4.

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J. Bernal and F. Escobar del Rey

ABSTRACT

Thyroidectomized rats were injected daily with 1.9 μg/100 g body weight of 125I-labelled L-thyroxine (T*4). When isotopic equilibrium was attained, half the experimental group was injected twice with 2 mg of propylthiouracil at a 24 h interval. Animals were killed 7 h after the last dose and the amounts of T*4 and labelled iodide and T3 in peripheral tissues were determined after extraction and paper chromatography. The amount of T3 derived from T4 is significantly lower in tissues of rats receiving PTU.

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F. Escobar del Rey and G. Morreale de Escobar

Among the different factors which may influence the peripheral needs for thyroid hormone, changes in environmental temperature seem to have been most extensively studied. Different workers in this field (Bondy et al., 1952, Leblond et al., 1952, Rand et al., 1952, Kassenaar et al., 1956) were able to show by different types of experiments, that prolonged exposure to low temperatures is accompanied by an increase in peripheral thyroxine requirement. Kassenaar et al. (1956) clearly showed that these experiments have preferably to be done on thyroidectomized, thyroxine maintained animals as compensatory action may mask the results when intact animals are used.

Contrary to this, very little is known about the influence of muscular exercise on the thyroxine disappearance rate: Bondy & Hagewood (1952) not only studied the effect of low temperatures, starvation and cortisone on the PBI

1. The first paper, on »The effect of environmental temperature on the blood protein

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F. Escobar del Rey and G. Morreale de Escobar

No conclusive evidence on the influence of muscular exercise on thyroxine disappearance rate has yet been obtained. Bondy & Hagewood (1952) found a significant decrease in the PBI of rats after swimming for two hours. They used intact and thyroidectomized, thyroxine maintained rats, the latter being used in order to avoid a compensatory action of the thyroid. Lashof, Bondy & Sterling (1954) were, however, unable to observe any difference in the PBI and in the slope of the I131 labeled 1-thyroxine disappearance curve of healthy subjects after walking for 14 miles or swimming at full speed for 15 minutes. The thyroid function in these subjects had been previously blocked with iodide. The authors also state that muscular exercise does not increase the peripheral needs for thyroid hormone and that the differences in the PBI of swimming and control rats found in their first experiment (Bondy & Hagewood, 1952) were

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F. Escobar del Rey and G. Morreale de Escobar

Continuing previous studies on the possible effect which hypermetabolism producing factors may have on the peripheral degradation of 1-thyroxine in the rat (Kassenaar et al., 1956, Escobar del Rey & Morreale de Castro, 1956 a, 1956 b), it appeared of interest to investigate the action of 2,4 dinitrophenol (DNP), which is known to produce hypermetabolism in several animal species (Thomson et al., 1935).

The well known finding of a lowering of the serum PBI following the administration of DNP was first reported for the rat by Wolf et al. (1950) and for man by Castor & Beierwaltes (1955). The concomitant finding of a sharply lowered serum PBI and an apparently unaltered thyroid function (Wolff et al., 1950) seemed to indicate a lack of response of the hypophysis to the low levels of circulating hormone, which was later confirmed histologically by Goldberg & Chaikoff (1951). The very extensive work carried out

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F. Escobar del Rey and G. Morreale de Escobar

ABSTRACT

The effect of BHDB is determined on: a) the rate and mode of disappearance of [131I] l-thyroxine in thyroidectomized, l-thyroxine maintained rats, and b) the concentration of iodine-containing compounds in the body and excreta of thyroidectomized rats, isotopically equilibrated with l-thyroxine or l-triiodothyronine. Labelled thyroxine is rapidly excreted into the intestines and faeces of BHDB-treated rats and this alteration precedes a much less marked decrease of the urinary radioiodide. In isotopically equilibrated rats it is shown that during the first few days of BHDB administration there is a decrease of the urinary iodide, which later reverts to normal or, in the case of triiodothyronine maintained rats, increases well above normal values. The alterations of urinary iodide excretion are more than accounted for by opposite changes in the faecal excretion of iodinated compounds. BHDB results in a depletion of the hormonal pool in the peripheral tissues of thyroxine-maintained rats, but this is not so in the case of triiodothyronine-maintained animals. It is concluded that there is more evidence in favour of the interpretation that BHDB alters the availability of the thyroid hormone to peripheral tissues than in favour of an inhibition of peripheral deiodinating systems. It is suggested that the marked loss of thyroxine from the body of BHDB-treated rats might be the underlying cause of its »antithyroxine« action.

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F. Escobar del Rey and G. Morreale de Escobar

Conclusive evidence on the effect of 2,4 dinitrophenol (DNP) on the rate of breakdown of thyroid hormone(s) is not available.

The plasma I131 labeled 1-thyroxine disappearance curves obtained by Goldberg and associates (1955) in intact, propylthiouracil treated rats under the influence of DNP, and the observation made by Castor & Beierwaltes (1956) that the serum PBI of an athyreotic, thyroid maintained patient, decreased after the administration of DNP, strongly suggest that peripheral factors influenced the level of circulating thyroid hormone(s). The influence of DNP on the I131 distribution pattern in thyroidectomized, 1-thyroxine maintained rats. 24 hours after the injection of I131 labeled 1-thyroxine was studied in an attempt to obtain sufficient information to allow definitive conclusions (Escobar del Rey & Morreale de Escobar, 1958 a).

It was found that, though the radioactivity of the serum was definitely lower in the DNP treated animals and this decrease was

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G Morreale de Escobar, MJ Obregon and F Escobar del Rey

The present comments are restricted to the role of maternal thyroid hormone on early brain development, and are based mostly on information presently available for the human fetal brain. It emphasizes that maternal hypothyroxinemia - defined as thyroxine (T4) concentrations that are low for the stage of pregnancy - is potentially damaging for neurodevelopment of the fetus throughout pregnancy, but especially so before midgestation, as the mother is then the only source of T4 for the developing brain.Despite a highly efficient uterine-placental 'barrier' to their transfer, very small amounts of T4 and triiodothyronine (T3) of maternal origin are present in the fetal compartment by 4 weeks after conception, with T4 increasing steadily thereafter. A major proportion of T4 in fetal fluids is not protein-bound: the 'free' T4 (FT4) available to fetal tissues is determined by the maternal serum T4, and reaches concentrations known to be of biological significance in adults. Despite very low T3 and 'free' T3 (FT3) in fetal fluids, the T3 generated locally from T4 in the cerebral cortex reaches adult concentrations by midgestation, and is partly bound to its nuclear receptor. Experimental results in the rat strongly support the conclusion that thyroid hormone is already required for normal corticogenesis very early in pregnancy.The first trimester surge of maternal FT4 is proposed as a biologically relevant event controlled by the conceptus to ensure its developing cerebral cortex is provided with the necessary amounts of substrate for the local generation of adequate amounts of T3 for binding to its nuclear receptor. Women unable to increase their production of T4 early in pregnancy would constitute a population at risk for neurological disabilities in their children. As mild-moderate iodine deficiency is still the most widespread cause of maternal hypothyroxinemia in Western societies, the birth of many children with learning disabilities may already be preventable by advising women to take iodine supplements as soon as pregnancy starts, or earlier if possible.

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A. Aranda, F. Hervás, G. Morreale de Escobar and F. Escobar del Rey

ABSTRACT

Pituitary LH was studied by means of a specific radioimmunoassay (RIA) in male rats at different time intervals after thyroidectomy (T̄), and in rats which were T̄ at least 30 days before and were then treated with different doses of L-thyroxine or triiodo-L-thyronine.

A decrease in the pituitary LH of the T̄ animals, with respect to the intact age-paired controls, was demonstrable from 13 days after the operation, when total pituitary LH content was taken into consideration, or from 5 days after T̄, when the LH concentration (μg/mg pituitary) was considered. Doses of thyroid hormones lower than the daily maintenance dose for the rat produced very little effect on the pituitary LH levels of T̄ animals. However, a single dose of 1.75 μg of T4 or 0.2 μg of T3 (doses approximately equivalent to the T4 and T3 maintenance dose for T̄ rats) induced such a rapid and intense increase in the pituitary LH content that it no longer differed from that of the intact age-paired controls by 12 hours. Surprisingly, 5.0 μg of T4 and 1.0 μg of T3 did not produce any increase in the pituitary LH content of T̄ rats.

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F. Escobar del Rey, G. Morreale de Escobar, M. D. Garcia Garcia and J. Mouriz Garcia