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At least 1,081 records · Page 60Linked to original sources
PubMed1988

Catecholamine stimulation of cortisol secretion by 3-day primary cultures of purified zona fasciculata/reticularis cells isolated from bovine adrenal cortex.

Primary cultures of zona fasciculata/reticularis cells derived from bovine adrenal cortex secreted cortisol and corticosterone in response to isoprenaline, noradrenaline and adrenaline on the third day of culture. The potency order was isoprenaline greater than noradrenaline, adrenaline with an ED50 for all three agonists within the range 1-5 x 10(-8) M. A dose-dependent increase in medium content of cyclic AMP was also observed. Secretion of cortisol in response to these catecholamines was specifically blocked by propranolol but unaffected by phentolamine. The beta-agonist effect on cortisol secretion was specifically and progressively reduced, in a time- and dose-dependent manner, by pre-incubation of the cells with adrenaline.

Adrenal Cortex↗
PubMed1978

Protein kinase-mediated phosphorylation of a purified sterol ester hydrolase from bovine adrenal cortex.

Sterol ester hydrolase (cholesterol esterase, E.C. 3.1.1.13) of bovine adrenal cortex has been extensively purified by ammonium sulfate fractionation, acid precipitation, hydroxylapatite chromatography, and Sephadex G-200 chromatography. During the purification sequence, the hydrolase activity was purified free of endogenous protein kinase. With this purified preparation, activation by cyclic AMP and ATP-Mg2+ did not occur unless exogenous protein kinase was included in the activating system. Using [gamma-32P]ATP, the transfer of the terminal phosphate to the enzyme protein was demonstrated by three separate experimental approaches. With pooled fractions from Sephadex G-200 chromatography, significant binding of 32P by the enzyme protein was observed only in the presence of exogenous protein kinase. Time course studies disclosed a close concurrence between the extent of activation of the purified enzyme by cyclic AMP-dependent protein kinase and the level of 32P transfer from [gamma-32P]ATP to the enzyme protein. Finally, assays carried out during Sephadex G-200 chromatography showed a correspondence in the peaks for activated sterol ester hydrolase and for 32P binding by protein. The data confirm that activation of adrenal sterol ester hydrolase by cyclic AMP and ATP-Mg2+ involves protein kinase-catalyzed phosphorylation of the enzyme protein.

Adrenal Cortex↗
PubMed1976

[Histochemical study of the adrenal cortex of the rat after epiphysectomy].

The authors investigate the effects of pinealectomy on male rat's adrenal cortex. Fat material accumulates in the fascicular and reticular zones; different enzyme activities show light variations in operated animals. The frequent presence of mitochondrial multilamellar structures in pinealectomized rats is discussed.

Adrenal Cortex↗
PubMed1991

Effect of bombesin on the structure and function of the rat adrenal cortex.

Intact and dexamethasone-treated adult female Wistar rats were infused (Alzet osmotic minipumps) with bombesin (0.75 micrograms/rat per day) for 7 days. Bombesin depressed body weight and capacity of adrenal homogenate to secrete corticosterone; the latter effect was reflected in intact rats by a drop in serum corticosterone level. Bombesin had no effect on pituitary and serum adrenocorticotropic hormone (ACTH) concentration and serum aldosterone level. In intact animals, infusion of bombesin resulted in lowering of the number of parenchymal cells in adrenal cortex connected with the hypertrophy of glomerulosa and fasciculata cells. Moreover, bombesin lowered basal corticosterone secretion by isolated rat adrenocortical cells; however, neuropeptide applied did not change the response of isolated cells to ACTH stimulation. The data obtained clearly demonstrate inhibitory effect of bombesin on basal corticosterone secretion by the rat adrenal cortex.

Adrenal Cortex↗
PubMed1986

Absence of intermediate filaments in a human adrenal cortex carcinoma-derived cell line.

Subclones of a human adrenal cortex carcinoma-derived cell line (SW13) are described which by immunofluorescence lack detectable expression of any of the five known classes of intermediate filament (IF) proteins. Further investigation for vimentin and keratins in these subclones by two-dimensional gel analysis and by immunoblotting gave results consistent with the immunofluorescence results. Despite the apparent absence of IFs, SW13 subclones have organized actin and microtubule cytoskeletal networks, maintain an epithelial shape and colony pattern, and grow well in culture. Although a rat hepatoma cell line which similarly appears to have ceased IF expression has been reported, this is the first such report of a human cell line. Although rare, these cases provide evidence that IFs in general are not essential to growth in culture, nor are the keratin-containing IFs in particular necessarily responsible for the 'cobblestone' morphology or colony-type growth pattern characteristic of cultured epithelial cells.

Actins↗
PubMed1983

Unconjugated and sulfoconjugated steroids in plasma and zones of the adrenal cortex of the guinea pig.

The following steroids were measured in their unconjugated and sulfoconjugated forms in plasma and in the outer and inner zones of the adrenal cortex of the guinea pig: pregnenolone, 17-hydroxypregnenolone, 21-hydroxypregnenolone, dehydroepiandrosterone and deoxycorticosterone. In plasma, pregnenolone and 21-hydroxypregnenolone were the predominant unconjugated steroids with concentrations 10-30 times higher than the other three steroids. Among the sulfoconjugated steroids, pregnenolone sulfate had a concentration 25-50 times higher than the other sulfoconjugates. For each steroid except 21-hydroxypregnenolone the sulfoconjugated form was present in a concentration 2-7 times higher than the unconjugated form. In the adrenal cortex, the content of 21-hydroxypregnenolone was significantly higher in the outer zone than in the inner zone and was present in amounts 3-100 times greater than the other unconjugated steroids in the outer zone. On the other hand, the content of pregnenolone was significantly greater in the inner zone than the outer zone, and was present in amounts 3-80 times greater than the other unconjugated steroids in the inner zone. With the exception of 21-hydroxypregnenolone and deoxycorticosterone, the steroid sulfoconjugates were significantly higher in the inner cortical zone. As in plasma, pregnenolone sulfate was the most abundant sulfoconjugated steroid. This report also describes preliminary studies concerning sulfurylated hydroxyl groups in different positions of 21-hydroxypregnenolone. The sulfoconjugate was prepared by using partially purified steroid sulfotransferase from the guinea pig adrenal. The results obtained indicated that of the total 21-hydroxypregnenolone conjugate formed, approximately 40% was the 21-sulfate and 20% the 3-sulfate, whereas 40% was non-hydrolyzable with the techniques used and was not further characterized.

Adrenal Cortex↗
PubMed1991

Melatonin-induced suppression of the pinealectomy-stimulated rat adrenal cortex mitotic activity.

Pineal involvement in the regulation of adrenocortical mitotic activity has recently been suggested. It has been shown that melatonin (Mel) decreased the mean mitotic activity rate (MMAR) of the adrenal cortex both in vivo and in organ culture. The goal of the present study was to test the influence of pinealectomy (PX) and/or Mel-treatment on the MMAR of adrenocortical cells, as well as on the adrenal weight in rats. The stathmokinetic method was used in the study. It was found that PX significantly increased the MMAR of the adrenocortical cells. Moreover, Mel suppressed the proliferogenic effect of PX on the rat adrenocortical cells. Melatonin alone did not significantly affect the mitotic activity of the adrenal cortex. None of the three experimental procedures, i.e. Mel, PX and Mel-treatment of pinealectomized animals significantly affected the adrenal weight. The present data suggest that Mel may be involved in the inhibitory control of adrenocortical cell proliferation.

Adrenal Cortex↗
PubMed1992

[Adrenal cortex carcinoma: diagnosis, therapy and course in 10 cases].

Data from ten cases with carcinoma of the adrenal cortex, diagnosed between 1981 and 1988, have been extensively reevaluated. Six patients suffered from a hormonally active tumor with proven clinical and laboratory signs of hypercortisolism and/or hyperandrogenism. Female patients dominated the cohort (eight of ten). No preference for particular age (35 to 64, mean 52) or lateralisation of the tumor was recognisable. In all cases signs for endocrinopathy and/or tumor disease lead to investigative intervention. Nonspecific symptoms like pain, reduction of weight and fatigue were registered most frequently. In three patients an abdominal tumor was palpable. Investigation of hormone levels and imaging procedures (sonography and CT scan) assured correct diagnosis in all cases. Since prior to operation metastases have been detected in five cases and in eight cases capsular invasion was proven histologically only, one patient was free of tumor after operation but developed hepatic metastases later on. Altogether nine of ten patients developed metastases later on. Seven of the patients died from the perioperative period up to 8.4 +/- 8.15 months. Mean survival of all patients was 20.5 +/- 24.5 months. Histological grading and assessment of anaplasia did not correlate with either survival or tumor stage. None of the patients presented with tumor stage I according to the TNM system by MacFarlane (55). All four patients with advanced disease in stage IV died within the first year after operation. Eight patients were treated with 1 to 6 g of the adrenolytic o,p'DDD (mitotane, Lysodren). In one of these cases, a sonographically documented remission lasting for over eight years was observed. A second patient with anaplastic carcinoma showed a reduction of the size of pulmonary metastases under continuous therapy with o,p'DDD and a cyclic polychemotherapy. After the latter was discontinued, the course was progressive.

Adrenal Cortex Hormones↗
PubMed1990

Mechanism of corticotropin and cAMP induction of mitochondrial cytochrome P450 system enzymes in adrenal cortex cells.

We studied the kinetics of corticotropin (ACTH) induction of mitochondrial cytochromes P450scc and P450c11 and their electron transport proteins, adrenodoxin and adrenodoxin reductase, in bovine adrenal cortex cells in primary culture. The mRNA levels of these enzymes increase and reach a peak within 3-12 h after ACTH addition. The protein levels of adrenodoxin reductase and P450scc show an increase only nearly 24 h after ACTH addition. After ACTH addition, the intracellular level of cAMP reaches maximal levels within 5 min, and then decreases gradually over 60 min. Hence, we examined the effect of a pulse of ACTH or cAMP analogs on enzyme and mRNA levels. Exposure of the cells to ACTH for 1-2 h was sufficient for maximal induction of the enzymes and P450scc mRNA. In contrast, the induction of the enzymes and the mRNA by cAMP analogs or forskolin required the continuous presence of these agents for over 12 h. But, these agents stimulated cortisol secretion to the medium quickly, indicating that they can activate some intracellular processes while not showing any effect on enzyme induction. The absence of any effect of prolonged cAMP pulses on enzyme and mRNA levels weakens the previous hypothesis that cAMP is the sole second messenger for the ACTH induction of steroidogenic enzymes in adrenal cortex cells. The inductive ability of a brief pulse of ACTH indicates that ACTH can rapidly initiate a series of reactions that result in enzyme induction many hours later.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMedDate not supplied

Aging and the adrenal cortex.

Aging in humans is accompanied by an increase in adrenal glucocorticoid secretion and a decline in adrenal androgen synthesis and secretion. The intense interest in adrenal function in aging individuals in recent years is in large measure related to the potential impact of cortisol excess in the development of cognitive impairment and hippocampal neuronal loss, and to the desire to provide hormone replacement and healthy aging. Although the preliminary data is tantalizing, solid scientific evidence are not at hand. It is apparent that both issues are extremely complex. Dehydroepiandrosterone (DHEA) and its 3 beta-sulfate are fascinating molecules, including their synthesis and actions in the brain. Recent studies have shown that DHEA-sulfate (DHEA-S), but not DHEA, activates peroxisome proliferator-activated receptor alpha (PPAR alpha) in the liver, an intracellular receptor belonging to the steroid receptor superfamily. Thus, DHEA-S may serve as a physiological modulator of liver fatty acid metabolism and peroxisomal enzyme expression, and thereby may contribute to the anticarcinogenic and chemoprotective properties of this intriguing class of endogenous steroids. The life-sustaining role of adrenal cortisol secretion and its regulation of metabolism via catabolic actions may be modulated by its partner DHEA and DHEA-S. During the anabolic growth period (childhood and early adulthood) the body is exposed to relatively high levels of DHEA/DHEA-S but to relatively or absolutely high levels of cortisol during infancy and the aging phase. The cortisol/DHEA-S ratio during the life span follows a U-shape curve, which may be telling us to explore these two critical adrenal steroids in tandem.

Adrenal Cortex↗
PubMed1984

Adrenal cortex dysfunction: CT findings.

The computed tomographic appearance of the adrenal gland was studied in 302 patients with possible endocrinologic disease and 107 patients undergoing CT for nonendocrinologic reasons. Measurements of adrenal size were also made in 100 adults with no known adrenal pathology. CT proved to be a sensitive diagnostic tool in combination with clinical studies. When blood hormone levels are increased, CT can differentiate among homogeneous organic hyperplasia, nodular hyperplasia, benign adenoma, and malignant cortical adenoma. When blood hormone levels are decreased, CT can demonstrate hypoplasia or metastatic tumorous destruction. Calcifications or caseations can be demonstrated earlier than on plain radiographs. When hormone elimination is increased, the morphologic substrate can be identified; tumorous changes can be localized and infiltration of surrounding organs recognized.

Adenoma↗
PubMed1984

Characterization of steroidogenesis in cell cultures of the human fetal adrenal cortex: comparison of definitive zone and fetal zone cells.

The steroidogenic capacity of cells cultured from the definitive zone and fetal zone of the human fetal adrenal cortex was compared, using a serum-free medium without lipoproteins. Comparison of [3H]pregnenolone and [3H]progesterone metabolism in cultures from each zone incubated without ACTH indicated that only 3 beta-hydroxysteroid dehydrogenase, delta 4,5-isomerase (3 beta-HSD) activity was deficient in fetal zone cultures. Basal 3 beta-HSD activity was 3- to 5-fold lower in fetal zone cultures than in definitive zone cultures assayed after 3 or 10 days in culture. Although basal hydroxysteroid sulfotransferase activity was 2- to 4-fold greater in 3-day-old fetal zone cultures than in definitive zone cultures, this difference was not found in 10-day-old cultures due to a 3-fold decrease in fetal zone basal hydroxysteroid sulfotransferase activity. However, older cultures of fetal zone cells did maintain the characteristic high delta 5-steroid sulfate and low delta 4,3-ketosteroid basal production from [3H] pregnenolone as compared to definitive zone cultures. ACTH treatment for 48 h in serum-free medium increased the steroidogenic capacity of cell cultures from both zones and stimulated delta 4,3-ketosteroid production from [3H]pregnenolone and 3 beta-HSD activity in fetal zone cultures to levels characteristic of the definitive zone. These studies show that in the absence of ACTH the difference in steroidogenic capacity between the fetal zone and the definitive zone (due to the lower 3 beta-HSD activity in fetal zone cells) was maintained in cell cultures for a period up to 10 days.

3-Hydroxysteroid Dehydrogenases↗