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At least 397 records · Page 22Linked to original sources
PubMed1999

Proliferation and apoptosis in the human adrenal cortex during the fetal and perinatal periods: implications for growth and remodeling.

After 10-15 weeks of gestation, the human fetal adrenal cortex undergoes rapid growth due to enlargement of a specialized cortical compartment known as the fetal zone (FZ). Soon after birth, the FZ regresses and the adult zonation pattern develops at least in part from cells derived from the persistent definitive zone (DZ), a thin layer of tightly packed cells surrounding the FZ. We postulated that growth of the fetal adrenal cortex involves zone-specific cellular hyperplasia, whereas the postnatal involution of the FZ is due to apoptosis. Therefore, we investigated the pattern of cellular proliferation and death in the FZ and DZ of the human fetal and postnatal adrenal cortex using immunohistochemical staining for proliferating cell nuclear antigen as a marker of mitosis and in situ detection of DNA fragmentation as a marker of apoptosis. Between 10-14 weeks' gestation, the mitotic indexes (percentage of proliferating cell nuclear antigen-positive cells) in the DZ (26.46 +/- 2.95%) and in the FZ (21.26 +/- 2.57%) were not significantly different. Between 15-20 weeks gestation, the mitotic index increased significantly (P < 0.05) in both zones (FZ, 33.84 +/- 5.21%; DZ, 67.45 +/- 7.58%) relative to levels before 15 weeks. This increase persisted between 21-24 weeks gestation (FZ, 39.5 +/- 4.22%; DZ, 58.63 +/- 6.83%). Interestingly, after 14 weeks, the mitotic index of the DZ was significantly greater (P < 0.05) than that of the FZ. In adrenal specimens obtained from infants born prematurely and treated in utero with glucocorticoid, the mitotic indexes in the FZ and DZ were significantly decreased. At all stages of gestation, no apoptotic nuclei were detected in the DZ. However, scattered apoptotic nuclei were detected in the central portions of the FZ. The number of apoptotic nuclei in the inner FZ increased with advancing gestation and was maximal during the first postnatal month. To identify factors that may regulate apoptosis, primary cultures of midgestation FZ cells were treated with activin A and transforming growth factor-beta (TGFbeta). Activin A and TGFbeta both induced apoptotic cell death, as assessed by internucleosomal DNA cleavage (DNA laddering). Induction of apoptosis by activin A was prevented by concomitant addition of follistatin, an activin-binding protein. Taken together, these data indicate that 1) growth of the human fetal adrenal cortex involves cellular hyperplasia, mainly in the DZ and to a lesser extent in the FZ, which is probably dependent on ACTH; and 2) apoptosis occurs predominantly in the inner cortical compartment and may be responsible for the rapid regression of the FZ after birth, a process that may be regulated by activin A and/or TGFbeta.

Activins↗
PubMed1989

The effect of phenytoin on the corticoidogenesis in the mitochondria and the endoplasmic reticulum of bovine adrenal cortex.

In the mitochondria and endoplasmic reticulum of bovine adrenal cortex, the influence of phenytoin on corticoidogenesis was studied using 0.1 microCi 4-14C-cholesterol, 0.01 microCi 4-14C-17 alpha-hydroxyprogesterone, deoxycorticosterone and NADPH-generating system. The cholesterol side-chain cleaving activity in the mitochondria was facilitated by 0.1 microM phenytoin, but was inhibited by higher concentrations. Steroid 11 beta-hydroxylase activity was inhibited by phenytoin. The steroid 21-hydroxylase activity in the endoplasmic reticulum, on the contrary, was mildly stimulated by 1 and 10 microM phenytoin. Phenytoin formed a modified type I spectrum in the adrenocortical mitochondria-malate complex.

Adrenal Cortex↗
PubMed2006

[Effects of drugs on the adrenal cortex and its tumors].

The structure of the normal adrenal cortex is changed by stimulating hormones (ACTH) and inhibiting hormonal drugs (especially glucocorticoids). ACTH induces hyperplasia and lipid depletion in the fascicular and reticular zones, whereas glucocorticoids lead to atrophy and lipid accumulation in both zones. In animal experiments, the adrenostatic drug mitotane causes shrinkage of the cells of the fascicular and reticular zones, whereas metyrapone induces a decrease in the steroid producing organelle system and aminoglutethimide leads to an increase in lipids. In the therapy of patients with adrenocortical cancer, mitotane can cause an increase in of necrosis and fibrosis, but also in intracellular lipid. The ultrastructure shows increased liposomes, more pigment-rich lysosomes and laminated bodies.

Adrenal Cortex↗
PubMed1994

A specific binding site recognizing a fragment of angiotensin II in bovine adrenal cortex membranes.

We have characterized a specific binding site for angiotensin IV in bovine adrenal cortex membranes. Pseudo-equilibrium studies at 37 degrees C for 2 h have shown that this binding site recognizes angiotensin IV with a high affinity (Kd = 0.24 +/- 0.03 nM). The binding site is saturable and relatively abundant (maximal binding capacity around 0.5 pmol/mg protein). Non-equilibrium kinetic analyses at 37 degrees C revealed a calculated kinetic Kd of 47 pM. The binding site is pharmacologically distinct from the classic angiotensin receptors AT1 or AT2. Competitive binding studies with bovine adrenal cortex membranes demonstrated the following rank order of effectiveness: angiotensin IV (Val-Tyr-Ile-His-Pro-Phe) = angiotensin II-(3-7) (Val-Tyr-Ile-His-Pro) > angiotensin III (Arg-Val-Tyr-Ile-His-Pro-Phe) > or = angiotensin II-(4-7) (Tyr-Ile-His-Pro) > angiotensin II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe) > angiotensin II-(1-6) (Asp-Arg-Val-Tyr-Ile-His) > angiotensin II-(4-8) (Tyr-Ile-His-Pro-Phe) > > > angiotensin II-(3-6) (Val-Tyr-Ile-His), angiotensin II-(4-6) (Tyr-Ile-His), L-158,809 (5,7-dimethyl-2-ethyl-3-[(2'(1-H-tetrazol-5-yl)[1,1'-biphenyl]-4-y l) methyl]-3-H-imidazo[4,5-beta]pyridine H2O) and PD 123319 (1-[4-(dimethylamino)3-methylphenyl]methyl-5-(diphenylacetyl)4,5,6 ,7- tetrahydro-1H-imidazo[4,5-c]pyridine-6-carboxylic acid). The divalent cations Mg2+ and Ca2+ were shown to diminish the binding of 125I-angiotensioffn IV to bovine adrenal cortex membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1984

Sex differences in adrenocortical structure and function. XV. Cellular composition and quantitative ultrastructural study of adrenal cortex of adult male and female hamster.

Cellular composition of adrenal cortex of adult male and female hamster was evaluated and parallel quantitative ultrastructural studies were performed. The adrenal cortex of adult male hamster contained more parenchymal cells than that of female and the difference depended mainly upon the number of the zona glomerulosa and zona fasciculata cells. Moreover, cells and nuclei of the zona reticularis were markedly larger in male animals. Ultrastructural observations of both male and female adrenal glands did not reveal any significant difference; however, stereology showed that the volumes of mitochondrial compartment and membrane space, as well as the surface areas of mitochondrial cristae and smooth endoplasmic reticulum tubules were significantly higher in the male hamster zona reticularis cells. Cortisol output by adrenal slices and homogenates per unit weight of the gland was higher in male than in female hamster. On the ground of these data, it seems conceivable that the observed sex-differences in the rate of cortisol output by hamster adrenal gland depend upon the higher number of the zona fasciculata cells and larger size of the zona reticularis cells in male than female gland.

Adrenal Cortex↗
PubMed1987

The evaluation of adult females with testosterone producing neoplasms of the adrenal cortex.

Although uncommon, testosterone producing neoplasms of the ovary and the adrenal cortex occur periodically. Forty-seven instances involving the adrenal gland have been published since 1925; five, including the present patient, have occurred since 1981. Confusion concerning the site of the androgen secretion has been generated in the past because of limited roentgenographic study and the poor predicability of selective suppression or stimulating testing of the adrenal gland and the ovary. Of the 22 patients with testosterone producing neoplasms of the adrenal cortex reported since 1973, 45 per cent underwent needless ovarian surgical treatment prior to the correct diagnosis. By recognizing the significant correlation between a serum testosterone of 200 nanograms per deciliter or greater, a serum dehydroepiandrostenone of greater than 6,600 nanograms per milliliter coupled with a thorough pelvic examination, pelvic ultrasound and a more liberal use of high resolution computerized tomography of the adrenal gland, the correct diagnosis can be made. The patient presented herein illustrates the pitfalls inherent in the management of a patient with this problem.

Adolescent↗
PubMed1977

[Functional and structural changes in the adrenal cortex of rabbits under conditions of chronic inflammation of the prostate gland].

Investigation of the state of the rabbit adrenal cortex under conditions of depression of the incretory activity of the testicles resulting from chronic inflammation of the prostate showed progressive hyperplasia of the reticular zone of the adrenal cortex; as to the glomerular zone, it failed to display any marked pathological changes, and the fascicular zone demonstrated some signs of hypoplasia. Thus, the normal or elevated androgen excretion observed in the experimental male rabbits, was provided by an intensified activity of the reticular zone of the adrenal cortex, despite a decrease in testosterone biosynthesis in the testes.

Adrenal Cortex↗
PubMed1992

ACTH-induced ultrastructural changes in the zona fasciculata of the hamster adrenal cortex. Are intraadrenal thrombi regulators of corticosteroid secretion?

Correlated stereological and functional studies were performed on the effect of massive ACTH doses on adrenal cortex of the female hamster. ACTH resulted in a marked increase in adrenal gland weight at day 6 of treatment followed by a drop at day 9. Stereology showed significant enlargement of the zona fasciculata (ZF) cells with the highest value at day 6 and subsequent drop at day 9 of treatment. This hypertrophy was due to a notable increase in the volume of mitochondrial, SER, Golgi apparatus and lipid droplet compartments. Cortisol secretion by adrenal slices and homogenates was also highest at day 6 of ACTH administration and notably lower at day 9. At day 6 of ACTH treatment in outer ZF thrombi were seen. In their vicinity the subendothelial space was dilated and endothelial cells dissociated from the basal lamina. Numerous erythrocytes were also visible among dissociated ZF cells. At day 9 of experiment in outer part of ZF numerous spaces devoid of parenchymal cells appeared. The earlier authors considered the "empty spaces" or "holes" in hyperstimulated adrenal cortex as a sign of holocrine secretion of steroid hormones. The present findings enable us to introduce a new hypothesis on the development of these spaces. In our opinion in hyperstimulated adrenal cortex numerous thrombi may be formed leading thus to the degeneration of adrenocortical cells. Thus, the appearance of the "empty spaces" or "holes" in the gland is not connected with the holocrine secretion but with the regulation of the number of secretory cells in adrenal cortex by the thrombi-dependent mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed2000

Expression and regulation of melanocortin receptor-5 (MC5-R) in the bovine adrenal cortex.

Among the five members of the melanocortin receptor (MC-R) family, MC2 and MC5 are expressed in peripheral tissues. The receptor MC2 (ACTH receptor) almost exclusively expressed in the adrenal cortex whereas MC5-R is expressed in several organs including the adrenal cortex. Both receptors bind ACTH and activate adenylate cyclase. The aim of this work was to study the spatial distribution of MC5-R among the different zones of the bovine adrenal cortex and to analyze the regulation of its expression by its own ligands, ACTH and alpha-MSH and by angiotensin II (AII). Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and RNase protection assay, MC5-R was detected only in the glomerulosa zone whereas MC2-R was present in both glomerulosa and fasciculata zones of adult adrenal cortex. Treatments by ACTH, alpha-MSH, or AII increased the MC5-R mRNA level in glomerulosa cells by factors 7, 5, and 4.5, respectively. However, although potentially regulated by hormones, MC5-R is expressed at a level at least 100 times less than MC2-R, suggesting that MC5-R expression might only be at trace levels in grown adults, but could be much higher during embryogenesis.

Adrenal Cortex↗
PubMed1985

Steroidogenic characteristics of the adrenal cortex of the mare studied by electron microscopy.

The three concentric zones of the horse adrenal cortex (zonae glomerulosa, fasciculata and reticularis) showed marked interpenetration and exhibited a different relative development according to their position in the gland. Whereas the three cortical zones each had a specific histological structure, the ultrastructure of their cells showed a certain qualitative homogeneity. The differences corresponded essentially to the relative abundance of the constituents which are generally considered typical of steroidogeneous cells: mitochondria with vesicular cristae, smooth endoplasmic reticulum and lipid droplets. Their importance increased progressively from the zona glomerulosa to the zona reticularis. In this zone, the presence of gap and septate-like cell junctions, and mitochondria with vesicular cristae in close proximity to a smooth endoplasmic reticulum with numerous dilated tubules, suggested that steroidogenesis may be the most active. Ultrastructural findings were indicative of only quantitative differences between the steroidogenic capacities of the three zones of the mare adrenal cortex.

Adrenal Cortex↗