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Biomedical subjects

A S Belloni

Publications and source records attributed to A S Belloni.

At least 73 records · Page 4Linked to original sources
PubMed1982

Effects of ACTH on the zona glomerulosa of sodium-loaded timolol maleate-treated rats: stereology and plasma hormone concentrations.

The effect of chronic ACTH administration on the growth and aldosterone secretion of the zona glomerulosa of sodium-loaded timolol maleate-treated rats was investigated by stereological and radioimmunological techniques. Combined sodium loading and timolol maleate administration induced a significant atrophy of the zona glomerulosa and its cells. The plasma concentration of aldosterone was significantly decreased, while that of corticosterone did not vary. ACTH administration completely reversed zona glomerulosa atrophy, and the plasma concentration of corticosterone was noticeably enhanced, whereas that of aldosterone underwent a further decrease. This data suggests that in the absence of the other adrenoglomerulotrophic factors, ACTH stimulates the growth of the zona glomerulosa, but transforms its parenchymal elements to a functional fasciculata cell type.

Adrenal Glands↗
PubMed1982

Ultrastructural observations on the regeneration of adrenocortical autotransplants in the rat spleen.

The regeneration of adrenocortical autotransplants in the rat spleen has been investigated by light and electron microscopy. Up to the seventh day after implantation, adrenal grafts showed large areas of necrosis and contained many degenerating (apoptotic) adrenocortical cells, some mesenchyme-like poorly differentiated elements, and occasional viable parenchymal cells. These last cells possessed mitochondria with scanty tubular cristae and few profiles of smooth endoplasmic reticulum. After 15 days of regeneration, adrenal grafts were reduced in volume, but contained only viable adrenocortical cells; after 30-36 days, autotransplants were noticeably enlarged and surrounded by an evident connective tissue capsule. Regeneration was closely associated with the morphological differentiation of adrenocortical cells, which one month after transplantation were found to assume all the typical features of adult rat zona fasciculata elements (i.e. mitochondria with vesicular cristae, abundant smooth endoplasmic reticulum, some lipid droplets and a well developed Golgi apparatus).

Adrenal Cortex↗
PubMed1980

An ultrastructural stereologic study of the effects of angiotensin II on the zona glomerulosa of rat adrenal cortex.

The effects of angiotensin II on the rat zona glomerulosa were investigated by morphometric and radio-immunological methods. Short-term (1 h) angiotensin-administration induced lipid depletion in zona glomerulosa cells and a significant rise in the plasma aldosterone concentration. Chronic angiotensin-treatment provoked a noticeable increase in the volume of the zona glomerulosa and its cells, which was mainly due to the hypertrophy of smooth endoplasmic reticulum and mitochondrial compartment. In chronically treated animals the output of aldosterone in response to a short-term stimulation with angiotensin II displayed a significant increase. These findings are interpreted as indicating that angiotensin II is involved in the stimulation of the growth and steroidogenic capacity of the rat zona glomerulosa.

Adrenal Cortex↗
PubMed1979

Fine structure of the rabbit adrenal cortex and the effects of short-term ACTH administration.

The fine structure of the rabbit adrenal cortex was investigated. The parenchymal cells display the ultrastructural features of steroid-producing cells, and also contain numerous electron-dense bodies frequently located near intercellular canaliculi, when open into the subendothelial space. Short-term ACTH-administration induced a noticeable decrease in the volume of the lipid compartment in the cells of all three cortical zones and a significant increase in the volume of dense bodies in the cells of zona fasciculata and zona reticularis. The hypothesis that these dense bodies are secretory granules is discussed in the light of biochemical evidence showing that ACTH increases the concentration of both corticosterone and cortisol in the decapsulated-enucleated adrenal homogenate and does not affect the activity of two lysosome-marker enzymes (i.e., acid phosphatase and beta-glucuronidase).

Adrenal Cortex↗
PubMed1979

A stereological study of the trophic effects of the renin-angiotensin system on the rat adrenal zona glomerulosa.

Left renal artery stenosis increased and timolol maleate chronic administration decreased systolic blood pressure, plasma renin activity, and plasma aldosterone concentration, in adult male rats. In the hypertensive animals the volume of the zona glomerulosa, the volume and number of zona glomerulosa cells, as well as the volume of the mitochondrial compartment and the surface area of SER and mitochondrial cristae, were significantly increased. The volume of the lipid compartment was reduced, and several clumps of electron-dense granules appeared at the juxta-sinusoidal pole of the cells. Opposite results were found in the zona glomerulosa of the hypotensive rats, with the exception that the volume of the lipid compartment showed no significant change. These findings suggest that the renin-angiotensin system is involved in the maintenance and stimulation of the growth in the zona glomerulosa. Since in the hypertensive rats the increase in the volume density of electron-dense granules fits well with that in the intracellular concentration of aldosterone, the working hypothesis is that these granules are aldosterone-containing secretory organelles.

Adrenal Cortex↗
PubMed1978

High resolution autoradiographic investigations on the mechanism of the adrenolytic effect of 7,12-dimethylbenzanthracene on the inner layers of the rat adrenal cortex.

The effects of chronic treatment with DMBA on the 3H-uridine incorporation into rat adrenocortical cells was investigated by high resolution autoradiography. It was found that DMBA significantly decreases the tracer incorporation into both nuclear and mitochondrial compartments of the zona reticularis cells. The hypothesis that the mechanism of the lytic effect of DMBA on the inner adrenocortical layers involves inhibition of nuclear and mitochondrial RNA synthesis is discussed.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

An ultrastructural, morphometric and autoradiographic study of the effects of 7,12-dimethylbenzanthracene on the rat adrenal cortex.

The effects of chronic treatment (up to 9 consecutive days) with 7,12-dimethylbenzathracene (DMBA) on the adrenal glands of adult male Wistar rats were investigated. Morphometry showed that DMBA provokes atrophy of the zona reticularis which was due to the decrease in both cell volume and number. The zona fasciculata showed only a decrease in the cell volume, whereas the zona glomerulosa did not display any significant changes. Autoradiography demonstrated that DMBA induces a significant increase in the number of mitoses and "S" phase cells in the zona glomerulosa and outer zona fasciculata, which may be interpreted as a repair mechanism of the DMBA-provoked slight necrosis in the inner adrenocortical layers. The mechanism(s) underlying the cytotoxic effect of DMBA is discussed in the light of our ultrastructural observations showing that the chemical causes a decrease in the volume of the mitochondrial and nuclear compartments and in the surface of smooth endoplasmic reticulum as well as an increase in the volume of the lipid compartment.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Investigations on the turnover of adrenocortical mitochondria. X. A correlated biochemical stereological study of the effects of chronic treatment with chloramphenicol on the mitochondria of the rat zona fasciculata.

The effects of chloramphenicol (CAP) on rat adrenocortical cells were investigated by biochemical and stereological methods. It was found that administering 50mg/kg of CAP every 12 hours provoked a persistent inhibition of the incorporation of 3H-leucine into mitochondrial proteins. Chronic treatment (up to 15 consecutive days) with this dose of CAP induced a significant decrease in the volume of the mitochondrial compartment, in the surface area of the outer and inner mitochondrial membranes and in the number of mitochondria per cell. These results confirm the hypothesis that the ACTH-induced maintenance of adrenocortical mitochondrial growth requires continuous mitochondrial DNA-dependent protein synthesis.

Adrenal Cortex↗
PubMed1978

Cytogenesis in the rat adrenal cortex: evidence for an ACTH-induced centripetal cell migration from the zona glomerulosa.

The mechanism underlying cytogenesis in the adrenal cortex of ACTH-treated rats was investigated. ACTH was found to increase the number of parenchymal cells in the zona fasciculata as well as that of "S" phase cells in the inner half of the zona glomerulosa and in the outer third of the zona fasciculata. The fate of 3H-thymidine labelled cells in ACTH-administered rats was also autoradiographically followed. The results are consistent with the hypothesis that the ACTH-provoked hyperplasia in the zona fasciculata involves the centripetal migration of newly-formed parenchymal cells from the zona glomerulosa.

Adrenal Cortex↗
PubMed1977

Investigations on the turnover of adrenocortical mitochondria. VIII. A stereological study of the effect of chronic treatment with ACTH and dexamethasone on the morphology of mitochondria in zona glomerulosa cells of the rat.

The effects of chronic administration of ACTH and dexamethasone on the morphology of mitochondria in zona glomerulosa cells of the rat adrenal cortex were investigated by stereological techniques. It was found that the volume of the mitochondrial compartment as well as the surface of the outer and inner mitochondrial membranes were significantly increased or decreased in relation to the number of days of ACTH- or dexamethasone-treatment. In ACTH-administered rats, the average volume of individual mitochondria decreased significantly up to the 6th day of treatment and then showed a conspicuous increase from the 6th to the 15th day, whereas in dexamethasone administered animals this parameter, after a small increase during the first 6 days of treatment, displayed a significant decrease. The number of mitochondria per cell showed a dramatic increase during the first 6 days of treatment with ACTH and continued to increase, but only slightly, with the subsequent treatment. In contrast, this parameter showed a parabolic decrease as a function of the duration of treatment in animals receiving dexamethasone. In the light of evidence showing that dexamethasone blocks ACTH-release, these findings are discussed and interpreted to indicate that ACTH is involved in the maintenance and stimulation of the growth and proliferative activity of mitochondria in rat adrenal zona glomerulosa.

Adrenal Cortex↗
PubMed1977

Investigations on the turnover of adrenocortical mitochondria. VI. An autoradiographic study of the effect of ACTH on the radioactivity decay in the mitochondrial compartment from the zona fasciculata of 3H-thymidine injected rats.

The radioactivity decay of the mitochondrial compartment from the zona fasciculata of the adrenal cortex of 3H-thymidine-injected rats was followed by high resolution autoradiography. The number of days in which the radioactivity of the mitochondrial compartment was reduced to a half was calculated from the semilogarithmic plots of radioactivity versus time. Since DNA is a very stable molecule, it was assumed that this parameter can be an estimate of the half-life of adrenocortical mitochondria. The half-life of mitochondria from the zona fasciculata of the normal rat averaged 11.17 days, and ACTH was found to increase significantly this figure to about 15 days. It is hypothesized that the ACTH-elicited stimulation of the growth of rat adrenal zona fasciculata mitochondria involves not only hypertrophy and proliferation of the organelles (Nussdorfer et al., '74b), but also the slowing down of the degeneration rate of mitochondria.

Adrenal Cortex↗
PubMed1977

Investigations on the turnover of adrenocortical mitochondria. XI. Effects of dexamethasone on the half-life of mitochondria from the rat zona fasciculata.

The effects of dexamethasone on the half-life of rat adrenocortical mitochondria were investigated by high resolution autoradiography and liquid scintillation spectroscopy. According to the method employed, the half-life averaged 11.27 and 10.46 days. Dexamethasone was found to decrease significantly this parameter (to about 5 days). Since dexamethasone-treated rats can be regarded as pharmacologically hypophysectomized animals, the data indicates that ACTH is involved in the maintenance of the half-life of adrenocortical mitochondria.

Adrenal Cortex↗
PubMed1977

Effects of ACTH and dexamethasone on the zona glomerulosa of the rat adrenal cortex: an ultrastructural stereologic study.

The effects of a chronic treatment with ACTH and dexamethasone on the zona glomerulosa of intact rat adrenals were investigated by morphometric methods and electron microscopy. It was found that ACTH increases the volume of the zona glomerulosa, of the cells, nuclei mitochondrial compartment as well as the surface of SER and mitochondrial compartment as well as the surface of SER and mitochondrial cristae. Also noticeable was the hypertrophy of the Golgi apparatus. Opposite effects were obtained after dexamethasone treatment. These findings are interpreted as indicating that ACTH is involved in the maintenance and stimulation of the growth and steroidogenic capacity of the adrenal zona glomerulosa.

Adrenal Cortex↗
PubMed1976

Investigations on the turnover of adrenocortical mitochnodria. VII. Effects of ACTH on the half-life of mitochondria from the zona reticularis of the rat adrenal cortex.

The half-life of mitochondria from the zona reticularis of the rat adrenal was calculated by determining the radioactivity decay curves of the mitochondrial compartment of 3H-thymidine-injected animals, using autoradiographic methods. ACTH was found to enchance significantly the half-life of the organelles.

Adrenal Cortex↗
PubMed1976

Investigations on the turnover of adrenocortical mitochondria. IV. A stereological study of the effect of chronic treatment with ACTH on the size and number of rat zona reticularis mitochondria.

The effects of chronic administration of of ACTH (up to 36 consecutive days) on the mitochondria of the zona reticularis of the rat adrenal cortex were investigated by stereologic techniques. It was found that ACTH induces two phases of hypertrophy of mitochondria alternating with two proliferative stages, which are associated with a significant decrease in the average volume of the organelles. It is suggested that, as in the zona fasciculata, ACTH controls the processes of growth and division of mitochondria in the zona reticularis. The mechanism underlying this action of ACTH as well as the differences between the responses to ACTH of the mitochondrial population of the two adrenal zones are discussed in the light of evidence indicating that mitochondria contain a complete genetic apparatus largely independent of nuclear control.

Adrenal Cortex↗
PubMed1976

Effect of ACTH on the zona reticularis of the rat adrenal cortex: an ultrastructural stereologic study.

The effects of ACTH on the rat adrenal zona reticularis were investigated by stereologic methods. It was found that the zona reticularis cell responsiveness to ACTH is similar to that of the zona fasciculata elements. This excludes that the zona reticularis of the adult rat can only function as the site of destruction of worn-out elements migrating from the adrenal outer zones.

Adrenal Cortex↗
PubMed1975

Investigations on the turnover of adrenocortical mitochondria. III. Stereologic and autoradiographic observations on the effect of chronic treatment with dexamethasone on the rat Zona fasciculata mitochondria.

The effects of chronic administration of dexamethasone (for up to 15 consecutive days) on both the morphology and DNA-synthesis of the mitochondria of the rat adrenal zona fasciculata were investigated by stereologic and autoradiographic techniques. Up to the 3rd day of continuous dexamethasone treatment, the average volume of mitochondria did not change, whereas the number of mitochondria per cell was significantly decreased. From the 3rd to the 15th day of hormonal administration both the volume and number of mitochondria were found to decrease in proportion to the duration of treatment. Autoradiography showed that after the 3rd day of dexamethasone administration there is virtually no incorporation of 3H-thymidine into the mitochondrial compartment. These findings are discussed in the light of evidence indicating that dexamethasone blocks ACTH-release by inhibiting the hypothalamo-hypophyseal axis. The results confirm the view that ACTH controls the maintenance of growth and proliferation of rat adrenocortical mitochondria.

Adrenal Cortex↗