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SUMMARY
Transmucosal electrical potential difference and short-circuit current of an in-vitro preparation of mucosal epithelium of rat colon were almost abolished and active sodium transport ceased when ouabain (1 mmol/l) was present on the serosal side of the epithelium.
A considerable fraction of the total ATPase activity in the mucosa was sodium dependent and concentrations of ouabain of 0·5 mmol/l or more completely eliminated the activity of this fraction.
Adenosine triphosphatase activities in mucosa taken from normal, hypothyroid, aldosterone-treated and sodium-depleted rats were compared. The activity of the ouabain-sensitive, sodium-dependent fraction was similar in all groups except for the hypothyroid rats in which it was considerably reduced.
There was no evidence from the present study that the increased active sodium transport by colonic mucosa, associated with aldosterone action or sodium depletion, depended upon a change in ATPase activity. In hypothyroidism, reduction of ouabain-sensitive ATPase activity may be responsible for the observed impairment of the sodium transport mechanism.
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SUMMARY
Rats were given a continuous intravenous infusion of aldosterone for up to 16 days. The rate of urinary Na+ excretion was initially depressed, but 'escape' occurred in about 4 days. Diurnal variation of Na+ excretion rate persisted even when the Na+ intake rate was controlled by infusion and when there was a continuous high level of exogenous aldosterone. After stopping aldosterone infusion, a transient rise in the rate of Na+ excretion was observed. Colonic transepithelial potential difference remained elevated as long as the infusion was continued and the short-circuit current, which is largely accounted for by active Na+ absorption, was increased. Stool Na+ content was reduced. The Na+ transport system of colonic epithelium, unlike that of kidney, does not appear to escape from the effect of aldosterone.
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Three different methods were compared for 125I-labelling of thyroid-stimulating hormone (TSH) for use in receptor-binding studies with human thyroid membranes: these were the chloramine-T, Bolton–Hunter and lactoperoxidase methods. Chloramine-T proved to be an inferior method to the other two. Iodinations to different specific activity (0·7–9·4 Bq/pg) were also compared: too high a specific activity led to reduced binding and a dramatic shift in the pH optimum for the TSH–receptor interaction.
A specific activity of 2·5 Bq/pg should not be exceeded if binding of 125I-labelled TSH is to be representative of the binding of the natural hormone. Under these conditions, pH 7·5 was optimal for binding of TSH to its receptor. Repurification of the labelled TSH by receptor adsorption also proved to be essential.
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SUMMARY
High levels of labelled serum protein were found in rats with hypertrophied and colloid-depleted thyroids, but only after high thyroid irradiating doses of 131I. Low levels were found in rats with normal thyroids after low or high thyroid irradiating-doses of radioactive iodine. The levels in rats with hypertrophied thyroids after low thyroid-irradiating doses of 125I did not differ greatly from those in rats with normal thyroids. The mechanism of serum protein labelling is discussed and it is suggested that similar conditions may be important for the production of high levels of labelled serum protein in patients treated with radioactive iodine for functioning thyroid carcinoma.
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SUMMARY
Radio-iodide was administered by prolonged continuous intravenous infusion to rats maintained under iodine-replete conditions and in moderate iodine deficiency. A close approximation to equilibrium labelling was thereby achieved. Labelled iodocompounds extracted from various tissues were analysed by thin-layer chromatography.
Moderate iodine deficiency resulted in a slight increase in the ratio of mono-iodotyrosine to di-iodotyrosine in the thyroid. No change in the ratio of tri-iodothyronine (T3) to thyroxine (T4) was found in thyroid, plasma or skeletal muscle. Faecal excretion of T3 declined appreciably relative to that of T4.
Under iodine-replete conditions the ratio of thyroidal secretion rates of T3 and T4 was estimated to be more than three times higher than the ratio of these iodocompounds within the thyroid. Heterogeneity of thyroglobulin structure and function may explain these observations.
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SUMMARY
Extrathyroidal tissues of the rat were labelled to steady state by prolonged continuous intravenous infusion of 125I-labelled thyroxine (T4) or tri-iodothyronine (T3). Labelled iodocompounds extracted from various tissues were analysed by thin-layer chromatography.
Significant amounts of labelled T3 were found in all tissues examined after infusion of [125I]T4, confirming that conversion of T4 to T3 occurs in extrathyroidal tissues of the rat. Faecal excretion of labelled T3 after [125I]T4 infusion provided an assessment of the extent of extrathyroidal conversion: about a third of the T4 was metabolized by this pathway. Extrathyroidal conversion was independently estimated to account for about a third of the total production of T3.
The site of extrathyroidal conversion was established by comparing the distributions of labelled T3 after the two types of infusion: kidney and liver were both prominent sites of conversion of T4 to T3.
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The binding of 125I-labelled bovine TSH (bTSH) to a wide range of human thyroid membrane preparations was compared with that of 125I-labelled human TSH (hTSH). Much higher binding percentages were obtained with the 125I-labelled bTSH. This was because the receptors had a higher binding affinity for bTSH than for hTSH. No differences in tracer purity, nor differences in optimal conditions for the binding of bTSH or hTSH, nor tracer degradation contributed significantly to the better binding of 125I-labelled bTSH.
Good correlation was found between binding percentages for 125I-labelled bTSH and 125I-labelled hTSH over the range of thyroid specimens. Useful information on human TSH receptors is, therefore, obtainable from binding studies with 125I-labelled bTSH.
The TSH displacement curves yielded linear Scatchard plots whenever the tracer and displacing hormones were of the same species. The data were, therefore, consistent with a simple binding reaction between TSH and a single set of independent receptor sites.
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SUMMARY
Transmucosal electrical potential difference (p.d.), short-circuit current, electrical resistance and Na+ influx rate of the descending colon were similar in euthyroid and hypothyroid rats, the latter having been treated earlier with an ablation dose of 131I. However, in contrast to the considerable p.d. increase found in normal rats, little change of p.d. was found in hypothyroid rats when they were Na+ depleted or given an intravenous aldosterone infusion. A single small dose of tri-iodothyronine (T3) (1 μg/100g body weight) or a larger dose of thyroxine given to hypothyroid rats 10–16 h before aldosterone, restored the p.d. response to normal, although these doses did not influence the animal's oxygen consumption. Fasting for 3 days or giving actinomycin D (8 μg/100 g body weight) abolished the effect of T3 but this did not influence the action of aldosterone in euthyroid animals.
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Testes from mature rats, rabbits, hamsters, guinea-pigs and dogs were perfused in vitro with added gonadotrophins to study the qualitative and quantitative aspects of oestrogen secretion by these species. After separation by high performance liquid chromatography (HPLC), the major oestrogen secreted by the testes of all five species was oestradiol-17β; lesser amounts of oestrone were also detected for all species. Secretion rates of oestradiol and testosterone were determined for one testis from each of six animals of each species after purification by HPLC. Oestradiol and testosterone secretion varied (P < 0·05) among species on both per testis and per gram of testis bases. The rabbit, which was a high secretor of oestradiol, was used in subsequent experiments to study the factors which affect short-term oestradiol secretion by perfused testes. Luteinizing hormone (NIAMDD-LH-S21) at 100 ng/ml significantly stimulated oestradiol secretion by 2·9-fold and increased testosterone secretion by 155-fold. Follicle-stimulating hormone (NIH-FSH-S11) had no significant effect on secretion of either steroid. In a time-course study in which LH stimulation was started after 45 min of control perfusion, the rates of increase in oestradiol and testosterone secretion over time were similar. Increasing amounts of testosterone added directly to the arterial perfusion medium (0–10 μg/ml) resulted in an increase in oestradiol secretion in the absence of gonadotrophins. Oestradiol secretion increased in a dose-dependent manner up to 1·0 μg testosterone/ml; there was no further stimulation of oestradiol secretion at 10 μg testosterone/ml. When testes were perfused with saturating concentrations of testosterone (10 μg/ml) neither LH nor FSH at 100 ng/ml increased oestradiol secretion above control values. It appears that the major factor affecting oestradiol secretion by in-vitro perfused rabbit testes is the amount of substrate (testosterone) available for aromatization.
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ABSTRACT
Among the processes contributing to the progressive acquisition of the highly malignant phenotype in breast cancer are ovarian-independent growth, antioestrogen resistance and increased metastatic potential. We have previously observed that increased invasiveness and development of ovarian-independent growth occur independently. In an attempt to define the inter-relationships between these processes further, we have compared the phenotypes of ovarian-independent, invasive and antioestrogen-resistant sublines of the ovarian-dependent human breast cancer cell line MCF-7. Cells acquiring ovarian-independent growth can retain sensitivity to anti-oestrogens. One clone of MCF-7 cells selected for stable antioestrogen resistance has become non-tumorigenic but its invasive potential remains unaltered. Thus, acquisition of some characteristics of the progressed phenotype can occur independently. This phenomenon of independent parameters in phenotypic progression could partly explain the considerable intra- and intertumour heterogeneity characteristic of breast tumours.
Journal of Endocrinology (1989) 122, 331–340
