Biomedical subjects

C Robba

Publications and source records attributed to C Robba.

At least 55 records · Page 3Linked to original sources

PubMed1981

Investigations on the turnover of adrenocortical mitochondria. XVII. A correlated stereological and autoradiographic study of the effects of chronic treatment with ethidium bromide on the growth of the rat zona reticularis mitochondria.

The effects of the prolonged administration of ethidium bromide (EB), at a dose provoking a persistent inhibition of the incorporation of 3H-thymidine and 3H-uridine into the mitochondrial fraction, on the zona reticularis of ACTH-treated rats were investigated. Stereologically, it was found that EB induces noticeable decrease in the total amount of the mitochondrial compartment, mainly due to the reduction in the number of organelles per cell. High resolution autoradiography showed that the mechanism underlying this effects of EB probably involves both the inhibition of mitochondria proliferation and the acceleration of their breakdown as "intact units". These findings suggest that the ACTH-induced maintenance of the zona reticularis mitochondria growth involves mitochondrial DNA reduplication and transcription.

Adrenal Cortex↗

PubMed1981

Effects of angiotensin II on the zona fasciculata of the rat adrenal cortex: an ultrastructural stereologic study.

The effects of a chronic administration of angiotensin II on the zona fasciculata of rats treated with dexamethasone and maintenance doses of ACTH were investigated by morphometric methods applied to electron microscopy. It was found that angiotensin induced a significant increase in the volume of cells, nuclei, mitochondrial and lipid compartments as well as in the surface area of smooth endoplasmic reticulum and mitochondrial cristae. Noticeable also were the hypertrophy of the Golgi apparatus and the increase in the number of acid phosphatase-positive dense bodies. These findings are interpreted as indicating that the renin-angiotensin system is involved in the stimulation of the growth and steroidogenic capacity of the rat zona fasciculata.

Adrenal Cortex↗

PubMed1980

Investigations on the turnover of adrenocortical mitochondria. XIV. A correlated biochemical and stereological study of the effects of chronic treatment with ethidium bromide on the growth maintenance of the rat zona fasciculata mitochondria.

The effects of ethidium bromide (EB) on rat adrenocortical cells were investigated by biochemical and stereological methods. It was found that a treatment with ip. injections of 10 microgram/gm of EB every 12 hours induced a persistent inhibition of the incorporation of 3H-thymidine and 3H-uridine into the mitochondrial fraction, but not into the nuclear fraction. Chronic treatment with this dose of EB provoked in zona fasciculata cells of rats treated with maintenance doses of ACTH a noticeable decrease in the volume of the mitochondrial compartment (due to the decrease both in the number per cell and in the average volume of the organelles) and in the surface area of the mitochondrial cristae. These findings lend support to the hypothesis that the mechanism underlying the ACTH-induced maintenance of the growth of adrenocortical mitochondria involves mitochondrial DNA reduplication and transcription.

Adrenal Cortex↗

PubMed1980

Investigations on the turnover of adrenocortical mitochondria. XV. A stereological study of the effect of chronic treatment with angiotensin II on the size and number of the mitochondria in the zona glomerulosa of the rat.

The effects of a chronic treatment with angiotensin II (up to 15 consecutive days) on the mitochondria of the rat zona glomerulosa cells were investigated by electron microscopic and stereological methods. Angiotensin induced a significant increase in the volume of the mitochondrial compartment. Up to the 3rd day of treatment this was due only to the hypertrophy of the organelles, and from the 3rd to the 15th day exclusively to mitochondrial proliferation. The hypothesis that angiotensin controls the growth and proliferation of rat zona glomerulosa mitochondria is discussed.

Adrenal Cortex↗

PubMed1980

Ultrastructure of cortisol-secreting adrenal adenomata.

Two adrenocortical adenomata causing Cushing's syndrome were examined by electron microscopy. Adenomatous cells were arranged in islets and contained ovoid nuclei with a prominent nucleoli. Mitochondria were polymorphic and displayed tubular and lamelliform cristae. Some cells were apparently devoid of lipid droplets and possessed an exceedingly well developed SER, the tubules of which were intermingled with small stacks of ribosome-studded cisternae, while other parenchymal cells contained large clumps of lipid droplets and scanty SER tubules. A conspicuous Golgi apparatus and many dense bodies of probable lysosomal nature were also observed. These findings suggest that the adenomata are derived from the zona fasciculata and that lipid-laden and lipid-free cells are, respectively, resting and actively secreting elements.

Adenoma↗

PubMed1980

Effects of human chorionic gonadotropins on the interstitial cells of the rat testis: A morphometric and radioimmunological study.

The effects of human chorionic gonadotropins (hCG) on the rat testicular interstitial cells (Leydig cells) were investigated by stereologic and radio-immunological methods. Short-term (2 h's) hCG-administration induced only lipid depletion in the Leydig cells. Chronic hCG-treatment provoked a significant cell hypertrophy, which was mainly due to smooth endoplasmic reticulum proliferation; the surface area of mitochondrial cristae, and the volume of the lipid and peroxisome compartments were also significantly increased. These morphologic findings are discussed in the light of radioimmunological data, showing that chronic hCG-administration increased the steroidogenic capacity (testosterone output) of the Leydig cells.

Animals↗

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

Investigations into the mechanism of progesterone release by rat lutein cells.

Vinblastine treatment blocks progesterone release from the lutein cells of superovulated immature rat ovaries, without impairing hormone synthesis, and induces the accumulation of electron-dense granules, 0.2--0.3 micron in diameter, at the juxta-sinusoidal poles of the cells. The hypothesis is advanced that these granules are true secretory organelles and that an exocytotic mechanism underlies the progesterone release from rat lutein cells.

Animals↗

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

Investigations into the mechanism of hormone release by rat adrenocortical cells.

Vinblastine treatment blocks corticosterone release from rat adrenal zona fasciculata without impairing hormone synthesis, and induces the formation of acid phosphatase-positive granular clumps at the juxta-sinusoidal pole of the cells. Autoradiography shows that ACTH administration to vinblastine-treated animals mobilizes the 3H-cholesterol stored in the lipid droplets and leads to a noticeable labelling of the granular clumps. The possible significance of these granules is discussed.

Adrenal Cortex↗

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↗

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 mitochondria. V. An autoradiographic study of the radioactivity decay in the mitochondrial compartment from the adrenal cortex of 3H-thymidine-injected rats.

The radioactivity decay of the mitochondrial compartment of 3H-thymidine-injected rats was followed by high resolution autoradiography. The number of days in which the radioactivity of the mitochondrial compartment is 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. It was found that the half-lives of mitochondria from the zonae glomerulosa, fasciculata and reticularis are, respectively, 8.20, 11.51 and 8.16 days.

Adrenal Cortex↗