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PubMed1976

Hepatic glucocorticoid binders in mature and senescent C57BL/6J male mice.

Because of prominent age-related changes in the responses to stress and in steroid metabolism and excretion, the effect of age on fractionated liver glucocorticoid-binding proteins was studied in C57BL/6J male mice. When cytosol, pre-labeled with [3H]corticosterone, was chromatographed on Sephadex G-100, 4 peaks were obtained. Peak 1 (excluded), peak 2 (corresponding to plasma transcortin), and peak 3 corresponding to glucocorticoid receptors isolated from nuclei) showed no significant age differences. This finding is consistent with reports that glucocorticoid-mediated induction of hepatic tyrosine aminotransferase is not altered by aging in rodents. However, there was a striking age-related decrease (80%) in peak 4 (apparent MW 29,000). Competition studies imply that peak 4 binds aldosterone, testosterone, progesterone, and corticosterone (delta4-3-keto steroids), but not estradiol or dt a plasma component. Although the function of peak 4 is not identified, the pattern of highest competition with delta4-3-keto steroids suggests that it is a steroid ring "A" reductase.

Adrenalectomy↗
PubMed1975

A radioreceptor assay for evaluation of the plasma glucocorticoid activity of natural and synthetic steroids in man.

An assay for plasma glucocorticoid activity has been developed using specific glucocorticoid receptors. Unlike other assays for cortisol and certain synthetic corticosteroids, this radioreceptor assay measures the glucocorticoid activity of all natural an synthetic steroids. Steroids extracted from as little as 0.05 ml of plasma are incubated with 3H-dexamethasone and cytosol receptors from cultured rat hepatome cells. From 0.5 to 50 ng of cortisol are accurately detected. Glucocorticoid activities of adult determined by the assay correlate closely with corticoid levels obtained in the CBG-isotope and fluorometric assays. Other steroids are measured in proportion to both concentration and potency as glucocorticoids. Relative activities include: cortisol 100, dexamethasone 940, prednisolone 230, prednisone 3, estradiol 1 and androstenedione 1. A similar ranking of steroids was found using receptors from a human source (fetal lung). The assay has been useful in detecting glucocorticoid activity in unidentified medications and in measuring plasma glucocorticoid levels after administration of synthetic corticosteroids. A modification of the assay is described for also estimating the level of free (unbound) glucocorticoid activity in plasma. Assays are performed before and after removal by charcoal of steroids not bound to plasma transcortin. This consideration is shown to be particularly important with prednisolone where the unbound steroid level is much less than the total. Thus, the radioreceptor assay provides a relatively simple technique for measuring the total of free plasma of glucocorticoid activity in man due to any natural or synthetic steroid or combination of steroids.

Aldosterone↗
PubMed1977

The effects of temperature and plasma cortisol on distribution of aldosterone between plasma and red blood cells: influence on metabolic clearance rate and on hepatic and renal extraction of aldosterone.

Aldosterone enters red blood cells (RBC) to a greater extent at 37 C than at lower temperatures. The ratio of 3H-aldosterone concentration in RBC to that in plasma increases from 0.2 at 4 C to 0.7 at 37 C when cortisol concentration is low. Increasing plasma cortisol increases the RBC/plasma aldosterone ratio. When plasma transcortin (CBG) is saturated with cortisol, the RBC/plasma ratio of 3H-aldosterone approaches 0.93, the ratio observed in RBC incubated in 4% albumin solution. The effects of plasma cortisol and temperature on the RBC/plasma ratio reflect an affinity of aldosterone for plasma CBG greater than the affinity for plasma albumin or RBC. Hepatic extraction averages 92% of plasma and RBC aldosterone. Neither hepatic extraction nor renal extraction (less than or equal to 20%) is significantly altered by changing plasma cortisol concentration. Whole blood MCR of aldosterone is unaffected by redistribution of aldosterone from plasma to RBC when plasma cortisol increases, but both plasma cortisol and the temperature at which blood is separated affect the RBC/plasma ratio of 3H-aldosterone and thus change the calculated plasma MCR. The RBC transport of aldosterone, and its dependence on temperature and plasma cortisol, must be taken into account in the evaluation of plasma aldosterone concentration.

Aldosterone↗
PubMed1978

Cytoplasmic and nuclear estradiol and progesterone receptors in human endometrium.

Estradiol and progesterone receptors have been characterized in normal human endometrial biopsy samples. The cytosol and nuclei were prepared from 150-250-mg samples, either processed immediately or kept in liquid nitrogen. The total concentration of estradiol-and progesterone-binding sites (available or occupied with endogenous hormone) were measured in both fractions. Results were best expressed in femto-moles per mg DNA, or in sites per cell, assuming an even distribution of receptor throughout the endometrial samples. The contribution to total binding of non-saturable binding components and of plasma proteins (transcortin or sex steroid-binding protein) was taken into account. Measurements were obtained in more than 300 patients, among whom 54 had completely normal menstrual cycles on the basis of clinical, hormonal, and histological features. Total estradiol and progesterone receptors were highest in the late proliferative phase (about 8,000 and 12,000 sites/cell, respectively) and were very significantly lower in the late secretory phase. During the proliferative phase, estradiol receptors were increased only in the nuclear fraction, whereas progesterone receptors were increased mainly in the cytoplasm. In the early luteal phase, estradiol and progesterone receptors decreased in the cytosol, whereas they remained high in the nuclei. Both receptors were at their lowest level in cytosol and nuclei in the late secretory phase. The changes of total estradiol and progesterone receptor sites and of their respective subcellular distributions seem to depend upon the plasma levels of both hormones and to follow the same cause and effect relationships as those demonstrated experimentally in laboratory animals.

Cell Nucleus↗
PubMed1979

A comparison of plasma protein changes induced by danazol, pregnancy, and estrogens.

Analysis of 25 plasma proteins was performed on blood drawn from 7 females before and during treatment with danazol. This steroid was found to induce a pattern of plasma protein changes similar to but not identical with that of other 17 alpha-alkylated anabolic steroids. For comparison, the same 25 plasma proteins were analyzed in blood from pregnant women in their third trimester, when the estrogen influence on plasma protein synthesis is most pronounced. Five major types of response were found. 1) Albumin and orosomucoid were not influenced by danazol or, after correction for volume expansion, by pregnancy. 2) Prealbumin, C1-esterase inhibitor, and haptoglobins increased substantially during danazol treatment but were not significantly influenced by pregnancy. 3) Transferrin, antithrombin III, prothrombin, and plasminogen showed marked increases after administration of danazol and during pregnancy. 4) Transcortin, ceruloplasmin, and alpha 1-antitrypsin doubled in pregnancy but were not influenced by danazol. 5) The concentrations of T4-binding globulin, pregnancy zone protein, and sex hormone-binding globulin more than doubled in pregnancy, and all three decreased to one third or less on administration of danazol. The plasma estradiol content fell correspondingly. The different types of plasma protein response found in these two groups of patients fit the hypothesis that hepatocytes contain steroid receptors capable of reacting with estrogens and/or other steroids such as danazol and, thus, influence the biosynthetic rate of many but not all plasma proteins according to a specific pattern. The synthesis of some of the estrogen-sensitive proteins is depressed after intake of danazol, which suggests that there is a competition for the receptors in the hepatocytes as there is for other estrogen target tissues.

Adult↗
PubMed1985

Endometrial and pituitary responses to the steroidal antiprogestin RU 486 in postmenopausal women.

The effects of the antiprogestin RU 486 on the human endometrium were investigated. Seventeen postmenopausal women were injected with estradiol (E2) benzoate (0.625 mg/day) for 15 days. Progesterone (P) (25 mg/day) and/or RU 486 (100 or 200 mg/day) were given to groups of 2-3 women during the last 6 days of E2 benzoate treatment. Serial blood samples were drawn for the measurement of plasma E2, P, and LH and FSH. An endometrial biopsy was performed on the last day of treatment, and processed for histology or for assays of DNA polymerase alpha, E2-dehydrogenase (E2DH), and P receptor (PR). Treatment with E2 benzoate alone resulted in a marked decrease of plasma gonadotropins; in those patients who received either P, RU 486, or both, in addition to E2 benzoate, the concentrations of plasma LH and FSH were further decreased to premenopausal levels. In absence of glycerol, the affinity of RU 486 for the endometrial PR (Kd = 0.8 nM) was higher than that of P (Kd = 1.2 nM). Glycerol decreased markedly the affinity of RU 486, whereas the affinity of P for the PR was unchanged. RU 486 had negligible affinity for plasma transcortin. Either P or RU 486, but not both together, induced secretory changes in the endometrium as determined from histologic sections of tissue biopsies. Either P or RU 486 decreased DNA polymerase alpha and increased E2-DH activities in the endometrium. Unexpectedly, when P and RU 486 were given together. E2-DH activity remained at the level found in E2-treated women. In vitro cultures of proliferative endometrium treated with the synthetic progestagen R 5020 or with RU 486 also had increased E2-DH activity; RU 486 counteracted R 5020 effects. We conclude that, contrary to previous results with experimental animals, the anti-P RU 486 has some progestomimetic activity in humans under specific conditions. Paradoxically, when given together with P, RU 486 lost most of its progestomimetic activity in the endometrium and behaved as a pure antagonist.

Adult↗
PubMed1986

Familial cortisol resistance: differential diagnostic and therapeutic aspects.

A 26-yr-old woman presented with hirsutism, male pattern scalp baldness ("geheimratsecken"), and menstrual irregularities. She had no hypertension or other signs and symptoms of Cushing's syndrome. Plasma cortisol levels were greatly elevated and did not suppress normally in response to dexamethasone. Cortisol binding to transcortin was normal. Plasma androstenedione and testosterone levels were also increased, but 17-hydroxyprogesterone and aldosterone levels were normal. Further studies revealed an increased cortisol production rate, increased 24-h urinary cortisol excretion, increased plasma ACTH levels, a normal diurnal rhythm of cortisol at an elevated level, and normal increments of plasma ACTH, cortisol, GH, and PRL in response to insulin-induced hypoglycemia. The father and two brothers also had increased plasma cortisol levels, which did not suppress normally in response to dexamethasone. Chronic therapy with dexamethasone (at first 1 and later 0.5 mg, three times daily) for more than 30 weeks resulted in decreased hirsutism, normalization of scalp hair and menstrual cyclicity, and normal plasma testosterone and androstenedione levels. No signs or symptoms of Cushing's syndrome developed, and the central regulation of secretion of ACTH, cortisol, GH, and PRL (insulin test, diurnal rhythm) remained qualitatively normal at a lower set-point. We conclude that this patient had autosomal dominantly inherited hereditary (partial) cortisol insensitivity, which had resulted in increased adrenocortical cortisol and androgen secretion. The latter had not resulted in clinical symptoms in the three afflicted male members of the family, but had in the propositus. The results also indicate the potential usefulness of the insulin test in distinguishing this disorder from Cushing's disease.

Adrenal Cortex Hormones↗
PubMed1975

Maternal and fetal plasma levels of free corticosteroids in pathological deliveries.

Does intrauterine acidosis induce increased steroid secretion? The concentration of free steroids (CS) increases in both fetal and maternal plasma during labor and delivery. Fetal levels are higher after vaginal than after cesarean section. These differences may indicate an important role of the fetal adrenal gland in the induction of labor or they may reflect merely the fetal response to the stress of delivery. During incrased intrauterine stress steroid secretion is increased as shown here. We examined 41 mothers and their infants during pathological labor. Pathology was assessed from fetal acidosis and/or a clinically obstetric disease of the mother or fetus. The 41 cases included 9 cesarean sections, 8 forceps deliveries; 24 spontaneous deliveries of which 7 were premature. At the time of delivery the pH and CS level were determined in maternal and umbilical vessels in all cases. During spontaneous labor blood samples were also taken during the different stages of labour. A competetive protein binding assay with transcortin without fractionation of the steroids was used. Progesteron was determined by the same assay. The level of this hormone, however, remains unchanged and hence any changes reflect changes in CS. The levels of CS were correlated with the pH values and compared to previously obtained normal values. During pathological deliveries CS levels in both mother and fetus are normal as long as there is no acidosis (Fig. 1). If acidosis is present the CS level in the umbilical artery is usually higher than normal. In 13 out of 18 vaginal deliveries the CS level was above normal, in the other 5 at the upper limit of normal (Fig. 1 and 2). At the same time the a--v difference becomes smaller and sometimes even negative. No changes were noted in maternal and umbilical venous blood (Tab. I and II). Similar dependence on the pH was found for cesarean sections (Tab. III). In premature deliveries without acidosis in the umbilical artery the CS levels were lower in both mother and fetus (Tab. I). These results indicate that the fetal adrenal gland reacts to acidosis, i.e., intrauterine stress, with increased corticosteroid secretion. This rise depends on the pH of fetal blood and not on the type of delivery (Fig. 3).

Acidosis↗
PubMed1984

Influence of oestrogen in high and low doses on plasma steroid concentrations in girls with tall stature and Turner syndrome.

Plasma DHA, 17-OH-progesterone, androstenedione, testosterone, cortisol, oestrone and oestradiol were determined before and on high dose oestrogen treatment (1, 3, 6 and 16 months) given to excessively tall girls to reduce future adult height. Basal values were normal: DHA 16.4 +/- 0.8 nmol/l (n = 90), 17-OH-progesterone 4.9 +/- 0.3 (n = 20), androstenedione 5.6 +/- 0.3 (n = 25), testosterone 2.6 +/- 0.3 (n = 24) and cortisol 395 +/- 20 (n = 90). On treatment, DHA, 17-OH-progesterone and androstenedione decreased to a minimum of 9.3 +/- 1.0 nmol/l (3 months, n = 13), 2.4 +/- 0.3 (6 months, n = 7) and 2.6 +/- 0.2 (6 months, n = 9), respectively, while testosterone remained unchanged, and cortisol increased to a maximum of 825 +/- 99 nmol/l (16 months, n = 23). In 15 girls with XO gonadal dysgenesis, basal DHA was low (11.8 +/- 1.0 nmol/l), and did not significantly change on low dose oestrogen replacement (13.3 +/- 1.4). The cause of the fall in plasma concentrations of androstenedione, DHA and 17-OH-progesterone in treated tall girls is unknown, but it is speculated that it might be related to peripheral conversion in the augmented adipose tissue mass. The rise in plasma cortisol, on the other hand, is probably due to increased transcortin.

Adolescent↗
PubMed1995

High-dose progesterone infusion in healthy males: evidence against antiglucocorticoid activity of progesterone.

High concentrations of unbound cortisol in late pregnancy have been explained by the antiglucocorticoid activity of high progesterone levels. To further test this hypothesis we studied the effect of high-dose progesterone on baseline and corticotrophin-releasing hormone (CRH)-induced hormone secretion in humans. In a double-blind crossover study eight healthy male volunteers received either progesterone (0.714 mg.kg-1.h-1 for 60 min followed by a dose of 0.45 mg.kg-1.h-1 over a total infusion time of 315 min) or vehicle as a continuous intravenous infusion. At 210 min a CRH test (0.1 microgram/kg body weight as bolus iv) was performed. Within 30 min after the start of progesterone administration the serum progesterone level increased to 454 +/- 31 nmol/l and remained in the range of third trimester pregnancy concentrations throughout the infusion period. During vehicle infusion the progesterone level remained in the normal range for healthy males and demonstrated a small but significant increase after CRH (1.52 +/- 0.23 vs 0.74 +/- 0.14 mmol/l; p < 0.01). However, baseline and CRH-stimulated serum cortisol and plasma adrenocorticotrophic hormone remained unaffected by high-dose progesterone. Moreover, unbound salivary cortisol also was not affected by progesterone, suggesting that there is no significant competition for transcortin binding sites. In conclusion, no antiglucorticoid activity was found after short-term administration of progesterone in males. These findings cast doubts on the concept that the alterations of the pituitary-adrenal axis in late pregnancy are induced by the antiglucocorticoid activity of high progesterone concentrations.

Adrenocorticotropic Hormone↗
PubMed1976

Corticosteroid binding by plasma proteins and the effects of oestrogens in the marsupial brush-tailed opossum, Trichosurus vulpecula (Kerr).

Using the techniques of equilibrium dialysis at 36 degrees C and gel filtration at 4 degrees C, a high-affinity, transcortin-like, corticosteroid binding system has been demonstrated in the blood plasma of the marsupial Trichosurus vulpecula. The affinity constant for non-albumin binding was 4-018 +/- 1-032 X 10(7) (S.C.) 1/mol for males and 4-046 +/- 0.981 X 10(7) for females. The concentration of non-albumin binding sites was 1-82 +/- 0.76 X 10(-7) mol/1 in males and 1-86 +/- 0-57 X 10(-7) mol/1 for females. Oestrogen administration, sufficient to cause marked hypertrophy of the genital tract in the femlaes, had no effect on the affinity constant or the concentration of the non-albumin binding sites in either males or females. The general condition of the animals deteriorated during oestrogen administration and there were significant falls in the concentrations of albumin and cortisol in the blood plasma. In one animal which died during oestrogen treatment, the adrenal glands were significantly hypertrophied.

Animals↗
PubMed1981

Effects of acute neurotrophic stress on peripheral metabolism of cortisol in conscious male guinea-pigs.

Cortisol metabolism was studied in conscious adult male guinea-pigs subjected to a neurotrophic stress (immobilization and stimulation by light for 3 h). The disappearance curves of tracer quantities of [3H]cortisol were represented by a two-pool model. In stressed animals, there was marked increase in the mean plasma level of cortisol (184% of control value; P less than 0.001) and in the metabolic clearance rate (MCR; 17% of control value; 0.001 less than P less than 0.001). This rise in the MRC of plasma cortisol resulted from an increase in the mean total apparent volume of distribution (49%, P less than 0.001). The lack of significant differences in the slopes of the second exponential phase of the disappearance curves indicated that the stress did not significantly increase the half-lie of cortisol. The mean binding capacity of transcortin for cortisol (ST) was significantly higher in the animals which had been subjected to the neurotrophic stress than in the control guinea-pigs (0.02 less than P less than 0.05). However, ST values remained very low and accounted for the very high levels of free cortisol found after the stress. The results suggest that the raised concentrations of unbound cortisol found in the plasma of conscious adult male guinea-pigs in response to neurotrophic stress reflect a hypersecretion of corticosteroid.

Animals↗
PubMed1988

Glucocorticoids in the blood plasma of the platypus Ornithorynchus anatinus.

Blood samples were obtained from two male and two female platypuses at various times after capture and anaesthesia for other experimental purposes. In samples obtained during ketamine-xylazine or pregnanediol anaesthesia 15-24 h after capture, the concentration of total glucocorticoids, measured as 'cortisol equivalent' in a radioligand assay, was 207-620 nmol/l. In samples taken 14-35 h after injection of dexamethasone (0.2 mg/kg) total glucocorticoid concentration was 79-88 nmol/l. Individual glucocorticoids were isolated on columns of Sephadex LH-20 and measured separately against appropriate standards. In all except two haemolysed samples obtained from a male that died 25 h after capture, the major glucocorticoid behaved as cortisol, contributing 77-94% of the total. The remainder was made up of varying proportions of substances behaving as corticosterone, 11-deoxycortisol and cortisone. In the haemolysed samples from the moribund animal the major reactive substance, contributing 52-54% of the total, behaved as cortisone. The total adrenal gland weight of this animal was 747 mg, compared with 200-286 mg in two others, suggesting preceding exposure to stress. Equilibrium dialysis and polyacrylamide gel electrophoresis (PAGE) revealed no evidence for a transcortin-like glucocorticoid- and progesterone-binding protein in platypus plasma. However, as in the echidna, there was a heat-labile, high-capacity binding system migrating with albumin on PAGE. Glucose was undetectable in the plasma of the moribund animal and only 1.7-2.8 mmol/l in the initial plasma samples from the others. In two animals, injection of glucose i.p. and dexamethasone i.m. was followed by an increase in the plasma concentration of glucose to the range 3.8-9.9 mmol/l and commencement of normal swimming and feeding activity for the next 36-48 h.

Animals↗
PubMed1990

Clinical pharmacokinetics of prednisone and prednisolone.

The growth of knowledge in the field of the pharmacokinetics of prednisolone/prednisone has been slow for several reasons. First, convenient and specific methods for measuring these steroids only became available with the development of high performance liquid chromatographic methods. Secondly, prednisolone is nonlinearly bound to transcortin and albumin: since the unbound concentrations of prednisolone are biologically relevant, it was necessary to determine the free fraction in each plasma sample. Thirdly, due to the short half-life of prednisolone no steady-state is achieved, and therefore area under the concentration-time curve needed to be determined in all studies. Fourthly, prednisolone and prednisone are interconvertible and prednisolone is given intravenously as an ester prodrug, features which created controversies about the correct interpretation of pharmacokinetic results. Finally, the total body clearances of total and (to a lesser degree) of unbound prednisolone increase with increasing concentrations of prednisolone. Therefore, in order to compare pharmacokinetic results between different subjects, standardised doses had to be administered. The investigations performed so far have revealed that: (1) the dose-dependent pharmacokinetics partly explain the clinical observation that an alternate-day regimen with prednisone yields fewer biological effects; (2) the interconversion of prednisone into prednisolone is not a limiting factor, even in patients with severely impaired liver function; (3) hypoproteinaemia per se does not cause increased unbound concentrations of prednisolone in vivo; (4) patients with liver failure, renal failure or a renal transplant, subjects older than 65 years, women on estrogen-containing oral contraceptive steroids or subjects taking ketoconazole have increased unbound concentrations of prednisolone-whereas hyperthyroid patients, some patients with Crohn's disease, subjects taking microsomal liver enzyme-inducing agents or patients on intravenous prednisolone phthalate (instead of prednisolone phosphate) or on some brands of enteric coated prednisolone tablets have decreased concentrations of prednisolone. The biological relevance of the altered pharmacokinetics is supported in part by altered clinical effects and altered effects on cellular immunofunctions.

Animals↗
PubMed1996

Plasma protein changes induced by two orally administered androgen derivatives.

Epostane is a synthetic 17 alpha-alkylated 5 beta-androstane derivative, active following oral administration and devoid of any apparent androgenic, estrogenic or antiestrogenic potency. Circulating concentrations of 13 different plasma proteins were measured in eight women before and after 2 and 4 weeks of daily oral intake of 600 mg of epostane. The results were compared with those previously found during administration of the same daily dose of danazol, a synthetic 17 alpha-alkylated androgen derivative with known androgenic/anabolic activity. Epostane significantly suppressed serum levels of sex hormone-binding globulin, pregnancy zone protein and thyroxin-binding globulin and increased the levels of transthyretin. Haptoglobins, plasminogen and transferrin showed minor and/or transient changes and the levels of high density lipoproteins, alpha2-macroglobulin, albumin, C1-esterase inactivator, C3 complement and transcortin remained unaffected. The pattern of changes in plasma proteins was almost identical to that induced by administration of danazol, although the effects of epostane were somewhat weaker. Thus epostane is capable of inducing substantial changes in the pattern of steroid-sensitive plasma proteins in an androgen-like fashion despite its apparent lack of androgenic activity. The capacity of a steroid to induce such changes thus seems to be tied to the chemical structure rather than to the intrinsic hormonal activity of the molecule.

Abortifacient Agents, Steroidal↗
PubMed1989

Chemotherapy and endocrine function in lung cancer.

To investigate whether cyclic chemotherapy for lung cancer influenced endocrine function, we monitored thyroxine, cortisol, testosterone, sex hormone binding globulin (SHBG), estradiol, FSH, LH, and transcortin every three weeks in 12 male patients. Treatment regimens consisted of cisplatin and etoposide in 9 patients, or vincristine, doxorubicin, and cyclophosphamide in 3 patients. SHBG and FSH level were significantly elevated after 6 to 9 weeks of therapy, whereas the other variables were unchanged. The results suggest that the therapy induces endocrine gonadal dysfunction. The increments in SHBG levels reflect a considerable fall in free testosterone, and may effect alterations in total androgen/estrogen ratios. The mechanism underlying the increased SHBG levels is unknown.

Aged↗
PubMed1987

Circadian rhythm in the membrane of circulating human blood cells: microviscosity and number of benzodiazepine binding sites. A search for regulation by plasma ions, nucleosides, proteins or hormones.

Circadian rhythms in both the number of peripheral type binding sites for benzodiazepines in platelet membranes and the microviscosity of the erythrocyte membrane were demonstrated in 7 healthy men. Neither variable appeared to be linked to each other, or regulated by the plasma concentrations of total or free cortisol, testosterone, potassium, magnesium, calcium, cAMP, cGMP or proteins or by the erythrocytic concentration of magnesium or potassium or by the plasma cAMP:cGMP ratio or by the ratio of intra-erythrocyte:plasma concentrations of potassium or magnesium. A highly significant negative correlation was found between the microviscosity of the erythrocyte membrane and the activity of the membrane-bound enzyme, methyltransferase I. Such a correlation was validated both on raw data and on 24 hr-means (r = 0.84; P less than 0.01). A circadian rhythm in the activity of this enzyme was also demonstrated. Moreover, a highly significant correlation was also found between plasma transcortin concentration (TRC) and microviscosity (r = 0.50, P less than 0.01), and between TRC and methyltransferase I activity (r = 0.61, P less than 0.01). Such findings may constitute clues towards the understanding of the regulation of the circadian rhythm in the fluidity of the red blood cell membrane in man and guide future steps with regard to the role of this rhythm upon the availability of drug binding sites at the cell surface.

Adult↗
PubMed1983

Decreased responsiveness of pituitary-adrenal axis to stress in vitamin A-depleted rats.

The functional ability of pituitary-adrenocortical system in relation to adequacy of vitamin A-nutriture was studied by comparing magnitude of its response to stress in vitamin A-depleted rats with that in normal animals. Repeated 4 h-daily immobilizations provoked a significant increase in urinary excretion of free plus conjugated transcortin-bindable corticosteroids with a concomitant rise in serum and adrenal content of free corticosteroids. In the vitamin A-depleted rats stress-evoked increase in urinary excretion and, serum and adrenal level of corticosteroids was less marked than those in the normal animals. The serum ACTH response to the stress was also decreased in the vitamin A-depleted rats. These results suggest that stress-induced activation of the pituitary-adrenocortical axis is significantly reduced in the vitamin A-depleted rats and that this depression is due, in part, to reduction of hypophyseal secretion of ACTH.

Adrenal Cortex Hormones↗