An ultrastructural stereological study of accessory adrenocortical glands in bilaterally adrenalectomised rats.
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Journal Article↗
Biomedical subjects
A S Belloni
Publications and source records attributed to A S Belloni.
Effects of 4-aminopyrazolo (3,4-d) pyrimidine on rat hepatocytes: an ultrastructural morphometric study.
The prolonged administration of the hypolipidemic drug 4-aminopyrazolo (3,4-d) pyrimidine (4APP) induced conspicuous morphological changes in rat hepatocytes, which are clearly demonstrated by stereology. We observed a significant decrease in the rough endoplasmic reticulum, and an accumulation of lipid droplets, which was coupled with a comparable rise in the hepatic concentrations of total cholesterol and triglycerides. These changes were interpreted as the expression of the 4APP-provoked impairment of the synthesis of the polypeptide chains of lipoproteins and of the consequent suppression of the assembly of lipid molecules in exportable lipoproteins. We also noted a neto lowering in smooth endoplasmic reticulum and peroxisomes, a decrease which was hypothesized to be the morphological counterpart of a reduced de novo cholesterol synthesis, due to the 4APP-induced rise in the intracellular cholesterol concentration.
Adenine↗
A morphometric study of the reversal of ACTH-induced hypertrophy of rat adrenocortical cells after cessation of treatment.
The effect of a prolonged (7-day) ACTH administration on rat zona fasciculata cells and its reversal after cessation of treatment was investigated by morphometry. ACTH treatment caused a notable cell hypertrophy, which was mainly due to the increase in the volume of the mitochondrial compartment and to smooth endoplasmic reticulum (SER) proliferation, and a conspicuous rise in the basal level of corticosterone. After cessation of ACTH administration, rat zona fasciculata cells underwent a time-dependent atrophy, so that after 5 days they resembled those of control animals, and the blood concentration of corticosterone reverted to the base-line value. The cell atrophy was provoked by the decrease in the volumes of the mitochondrial compartment and SER, and was associated with a striking time-dependent accumulation of dense bodies. Stereology demonstrated that during the first two days after ACTH withdrawal the decrease of SER prevailed over that of the mitochondrial compartment, while the reverse occurred during the remaining three days. The increase in the volume of dense-body compartment, though largely due to the accumulation of residual bodies, was mainly coupled with a rise in the volume of the microautophagic-vacuole compartment during the first two days after ACTH cessation and with an increase in that of the macroautophagic-vacuole compartment during the following three days. The hypothesis is advanced that both micro- and macroautophagy play a role in the reversal of ACTH-induced hypertrophy of rat zona fasciculata cells after cessation of treatment, the first process being mainly involved in the elimination of SER, and the second one in the degradation of mitochondria.
Adrenocorticotropic Hormone↗
Morphological and functional responses of rat Leydig cells to a prolonged treatment with human chorionic gonadotropins.
The morphological and functional responses of rat Leydig cells to a 3- and 6-day treatment with human chorionic gonadotropins (hCG) (10 IU/kg/day) were investigated by morphometric and radioimmunological techniques. hCG-administration induced a notable time-dependent enhancement in the steroidogenic capacity and growth of Leydig cells; this last was almost exclusively due to hypertrophy (and not to hyperplasia). The volume of mitochondrial and peroxisome compartments, as well as the surface area per cell of mitochondrial cristae and smooth endoplasmic reticulum (SER) were significantly increased after hCG treatment, and showed a highly significant positive linear correlation with both basal and stimulated testosterone production by isolated Leydig cells of the contralateral testis. Also the volume of nuclei and lipid-droplet compartment and the surface area per cell of Golgi apparatus displayed a notable hCG-induced rise, but they did not correlate with testosterone secretion. These findings suggest that, in addition to mitochondria and SER, in which the enzymes of steroid synthesis are located, peroxisomes are also specifically involved in the secretory activity of rat Leydig cells.
Animals↗
Effects of mevinolin, an inhibitor of cholesterol synthesis, on the morphological and functional responses of rat adrenal zona fasciculata to a prolonged treatment with 4-aminopyrazolo-pyrimidine.
Rat adrenocortical cells are almost completely dependent upon the continuous supply of cholesterol derived from serum lipoproteins. However, a prolonged (5-day) administration of 4-aminopyrazolo-pyrimidine (4-APP), a potent hypocholesterolaemic drug, though provoking a notable decrease in the intra-adrenal concentration of esterified and free cholesterol, did not significantly affect basal plasma level of corticosterone. Morphometry showed a conspicuous hypertrophy of zona fasciculata cells, coupled with a striking proliferation of smooth endoplasmic reticulum (SER) and peroxisomes and with a profound lipid-droplet depletion. The secretory response of zona fasciculata cells to ACTH was still present, but reduced by half with respect to control rats. The simultaneous administration of mevinolin, an inhibitor of cholesterol synthesis, to 4-APP-treated rats caused an additional drop in the intracellular content of free cholesterol and notably lowered basal plasma corticosterone concentration. Mevinolin magnified the 4-APP-induced zona fasciculata cell hypertrophy, as well as SER and peroxisome proliferation. The secretory response to ACTH was completely suppressed. These data are compatible with the view that the morphological changes, which rat zona fasciculata cells undergo during prolonged hypocholesterolaemia, are the expression of the activation of the endogenous cholesterol synthesis. This compensatory response, enabling zona fasciculata cells to maintain a normal basal rate of hormonal output and to respond (though less efficiently) to their main physiological stimulus, seems to be completely independent of any activation of the hypothalamo-hyphophyseal axis, since dexamethasone/ACTH treated rats were used. The hypothesis is advanced that the mechanism underlying this response may involve the decrease of the intracellular free-cholesterol pool.
Adenine↗
Effects of prolonged dopamine infusion on the zona glomerulosa of sodium-restricted rats treated or not with prolactin: stereology and plasma hormone concentrations.
Prolonged sodium restriction was found to induce a notable hypertrophy of rat zona glomerulosa (ZG) cells and a significant rise in the basal plasma aldosterone concentration. Chronic prolactin administration significantly furthered the effects of sodium restriction. Dopamine infusion (3 mg/kg day for 7 days) did not apparently affect ZG morphology and function in the control rats, while it significantly counteracted the effects of sodium deprivation combined or not with prolactin administration. However, the action of dopamine was less intense in sodium-deprived rats treated with prolactin. These findings confirm the view that the dopaminergic system exerts a tonic inhibitory effect, modulated by the sodium balance, on the growth and secretory activity or rat ZG. Moreover, they suggest that the mechanism(s) underlying the antiadrenoglomerulotrophic action of dopamine in rats only partially involve(s) the well-known suppression of the hypophyseal release of prolactin.
Adrenal Cortex↗
Effects of streptozotocin-induced experimental diabetes on the morphology and function of the zona fasciculata of rat adrenal cortex.
The effects of a severe streptozotocin (STZ)-induced diabetes on the morphology and function of the adrenal zona fasciculata were examined in rats with intact or pharmacologically interrupted hypothalamic-hypophyseal-adrenal axis. In animals with an intact hypothalamic-hypophyseal axis, STZ-diabetes induced hypertrophy of the cells of the zona fasciculata and a rise in the plasma corticosterone concentration. Conversely, in rats in which the hypothalamic-hypophyseal axis had been interrupted, experimental diabetes provoked atrophy of the zona fasciculata cells, and a lowering in the plasma corticosterone level. The effects of STZ-diabetes were completely reversed by insulin infusion in both groups of rats. The hypothesis is discussed that the chronic lack of insulin may directly inhibit the growth and steroidogenic capacity of the rat zona fasciculata and that this effect of experimental diabetes may be masked in rats with an intact hypothalamic-hypophyseal axis by the concurrent enhancement of ACTH release due to chronic stress resulting from the metabolic consequences of prolonged diabetes.
Animals↗
Evidence that long-term administration of a methionine-enkephalin analogue stimulates the growth and steroidogenic capacity of rat inner adrenocortical cells.
A prolonged infusion with D-ala2-met-enkephalinamide (DALA) caused a significant increase in both basal and ACTH-stimulated corticosterone secretion by dispersed inner adrenocortical cells of rats whose hypothalamo-hypophyseal axis was pharmacologically interrupted. This effect of DALA was associated with a notable hypertrophy of isolated cells. These findings suggest that enkephalins are involved in the stimulation of the growth and steroidogenic capacity of the cells of the inner layers of rat adrenal cortex.
Adrenal Cortex↗
Long-term stimulatory effect of neuropeptide-Y on the growth and steroidogenic capacity of rat adrenal zona glomerulosa.
A prolonged infusion with neuropeptide-Y (NPY) caused a notable hypertrophy of the adrenal zona glomerulosa and its parenchymal cells in rats whose hypothalamo-hypophyseal axis and renin-angiotensin system were pharmacologically interrupted. Zona glomerulosa hypertrophy was associated with a significant rise in both basal and stimulated plasma levels of aldosterone. Zona fasciculata cells and the blood concentration of corticosterone were not affected. These findings suggest that NPY is specifically involved in the stimulation of the growth and steroidogenic capacity of rat adrenal zona glomerulosa.
Adrenal Cortex↗
Effect of mevinolin on rat hepatocytes: a morphometric study.
A short-term (12 h) infusion with mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, significantly lowered plasma cholesterol concentration in rats. After 7 days of continuous treatment hypocholesterolaemia disappeared, and this was coupled with a notable increase in the average volume of hepatocytes. Liver-cell hypertrophy was associated with a striking proliferation of the membranes of both rough and smooth endoplasmic reticulum, as well as with a tremendous increase in the number of peroxisomes. These structural changes are interpreted as the morphologic counterpart of the compensatory response of rat liver to the prolonged inhibitory effect of mevinolin on cholesterol synthesis.
Animals↗
A morphometric study of the effects of melatonin on the rat adrenal zona glomerulosa.
The effects of a long-term administration of melatonin on the zona glomerulosa were investigated both in "normal" rats and in animals in which the hypothalamo-hypophyseal-adrenal axis and the renin-angiotensin system had been pharmacologically interrupted. Melatonin caused a notable hypertrophy of zona glomerulosa cells and a significant rise in the plasma concentration of aldosterone in both groups of rats. These findings indicate that melatonin exerts in vivo a strong direct stimulatory action on the growth and steroidogenic capacity of the rat zona glomerulosa.
Adrenal Glands↗
Zona glomerulosa morphology and function in streptozotocin-induced diabetic rats.
Streptozotocin-induced diabetic rats showed a significant lowering in both PRA (-31%) and basal plasma aldosterone concentration (-59%), coupled with a notable atrophy of the zona glomerulosa (-30%) and its parenchymal cells (-36%). Kalaemia and the blood level of ACTH were not affected. Insulin infusion reversed all the streptozotocin-evoked effects. Analogous, though less conspicuous, changes were induced by experimental diabetes also in rats whose hypothalamo-hypophyseal-adrenal axis and renin-angiotensin system had been pharmacologically interrupted by the simultaneous administration of dexamethasone-captopril and maintenance doses of ACTH-angiotensin II: the drops in the basal plasma aldosterone concentration and in the volume of zona glomerulosa and its cells ranged from -20% to -22%. In these animals, experimental diabetes significantly depressed the aldosterone response to the acute stimulation with angiotensin II (-55%), potassium (-50%), and ACTH (-43%). These findings indicate that the well known impairment of renin release may only partially account for the antiadrenoglomerulotrophic effect of experimental diabetes in rats. The hypothesis is advanced that the chronic lack of insulin may directly depress both the growth of the zona glomerulosa and the newly synthesis of some enzymes of aldosterone synthesis.
Adrenal Glands↗
An ultrastructural stereologic study of aldosterone secreting adrenal adenomas and of adjacent zona glomerulosa.
The ultrastructure of four aldosterone secreting adenomas and of the adjacent zona glomerulosa has been described by the use of stereological techniques. Adenomatous cells (about 2800 microns 3 in volume) invariably displayed a striking abundance of lipid droplets, which occupied about 30% of the cytoplasm. Mitochondria prevalently contained tubulo-lamellar or lamellar cristae, but some cells exhibited organelles with vesicular cristae. Smooth endoplasmic reticulum (SER) was not very abundant. Small lipofuscin-pigment granules were frequently seen and in a few cells they were exceedingly numerous. Zona glomerulosa cells were smaller (about 950 microns 3 in volume) and possessed mitochondria with typical tubulo-lamellar cristae, a plentiful SER and few lipid droplets. They showed the ultrastructural features of elements actively engaged in steroid synthesis. The possible origin of aldosteronoma cells from the zona glomerulosa is discussed.
Adenoma↗
A morphometric study of the effects of short-term starvation on rat hepatocytes.
Short-term (24 h) starvation induced a significant decrease in the liver weight and in the average volume of hepatocytes, together with a notable decrease in the hepatic concentration of proteins, glycogen, cholesterol and triglycerides. Hepatocyte atrophy was due for about 95% to the decrease in the membrane space, in which glycogen and endoplasmic reticulum membranes are contained, and for about 5% to the depletion of lipid droplets, in which cholesterol and triglycerides are stored. Nuclei, mitochondria and rough endoplasmic reticulum did not display appreciable modifications. The smooth endoplasmic reticulum underwent a net decrease, comparable with the decrease in the liver protein content, and the volume of dense-body compartment was increased, mainly through the rise in the number of microautophagic vacuoles and secondary lysosomes. These last findings were interpreted as the morphological counterpart of the fasting-induced enhancement of protein degradation in rat liver.
Animals↗
Investigations on the possible involvement of the dopaminergic system in the modulation of the growth and steroidogenic capacity of the rat adrenal zona glomerulosa: a coupled morphometric and biochemical study.
The effects of metoclopramide (MTC) and bromocriptine (BRC) (two drugs which act as antagonist and agonist of DOPA-receptors, respectively) on the zona glomerulosa of dexamethasone/ACTH-treated rats were investigated by coupled biochemical and morphometric techniques. Short-term (1-h) MTC administration significantly increased the plasma concentration of aldosterone, while long-term (7-day) MTC administration, as well as short- and long-term treatment with BRC did not cause any apparent change. Long-term MTC administration was found to significantly potentiate both the rise in the plasma level of aldosterone and the hypertrophy of the zona glomerulosa and its parenchymal cells induced by a prolonged treatment with angiotensin II (AII), but not those evoked by a chronic sodium deprivation alone or combined with AII infusion. Long-term BRC administration notably counteracted the effects of sodium restriction (coupled or not with AII infusion), but not those induced by the administration of AII alone. Long-term MTC administration partially reversed both the lowering of the plasma concentration of aldosterone and the atrophy of the zona glomerulosa and its parenchymal cells caused by a prolonged sodium-loading (combined or not with captopril infusion), but not those produced by the administration of captopril alone. On the other hand, long-term BRC treatment induced a further significant reduction in the blood level of aldosterone and the volume of zona glomerulosa and its cells only in captopril-treated animals. These findings are consistent with the view that the dopaminergic system exerts a maximal tonic inhibitory effect not only on the secretory activity, but also on the growth and steroidogenic capacity of the rat zona glomerulosa. Furthermore, they suggest that the activity of the dopaminergic system is in turn controlled by the sodium balance, being almost completely suppressed by a prolonged sodium deprivation.
Adrenal Cortex↗
The human adrenal cortex: ultrastructure and base-line morphometric data.
The morphology of the human adult female adrenal cortex was studied by electron microscopy and morphometry. Zona glomerulosa contains outer undifferentiated small cells and inner well-differentiated larger elements, which display mitochondria with tubulo-laminar cristae, abundant smooth endoplasmic reticulum (SER) and sparse lipid droplets. Zona fasciculata cells possess typical mitochondria with vesicular cristae, a well-developed SER, lipid droplets and some lipofuscin-pigment granules, which increase in number in the cells of the inner portion of the zone. Sometimes lipid-laden cells can be observed in the zona fasciculata. Zona reticularis cells have the same morphological features as the zona fasciculata elements, but display a striking rise in the number of lipofuscin-pigment granules.
Adrenal Cortex↗
Effects of the hypolipidemic drug nafenopin on the zona fasciculata of the rat adrenal cortex: a correlated biochemical and stereological study.
The effects of Nafenopin, a hypolipidemic drug, on the zona fasciculata of the rat adrenal cortex were investigated by biochemical, stereological, and cytochemical methods. Chronic Nafenopin treatment (5 days) significantly lowered serum cholesterol level, while it did not alter blood corticosterone concentration and 11beta-hydroxylase activity of adrenocortical cells. Stereology showed a significant increase in the average volume of zona fasciculata cells, which was almost exclusively due to smooth endoplasmic reticulum (SER) proliferation. The volume of lipid compartment was significantly reduced, whereas the volume of diaminobenzidine (DAB)-positive bodies (peroxisomes) per cell displayed a marked increase. Cholesterol administration per os to the treated animals raised the serum cholesterol level and completely reversed the Nafenopin effects. One day of Nafenopin administration provoked a slight but significant lipid depletion in adrenocortical cells, while 3 days of continuous drug treatment induced an extreme lipid depletion and a moderate increase in the SER coupled with a significant decrease in the plasma concentration of corticosterone. Since microsomal fraction and catalase seem to be involved in the cholesterol metabolism and utilization, the hypothesis is advanced that the Nafenopin-elicited SER and peroxisome proliferation is a compensatory response enabling adrenocortical cells to maintain an adequate level of hormonal output.
Adrenal Cortex↗
An electron-microscopic stereological study of the compensatory hypertrophy of the rat adrenal zona fasciculata after unilateral adrenalectomy.
The ultrastructural changes associated with the compensatory hypertrophy of the zona fasciculata cells on monoadrenalectomized rats were investigated by stereological techniques. It was found that these subcellular changes display a different pattern from those underlying the ACTH-induced adrenocortical cell growth in the intact rats. This result supports the view that compensatory adrenal hypertrophy does not involve activation of the hypothalamo-hypophyseal-adrenal axis.
Adrenal Cortex↗