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Biomedical subjects

G Mazzocchi

Publications and source records attributed to G Mazzocchi.

At least 199 records · Page 11Linked to original sources
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↗
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

Effects of ACTH and 3',5'-cyclic purine nucleotides on the morphology and metabolism of normal adult human adrenocortical cells in primary tissue culture.

Stereological studies showed that treatment of normal adult human adrenocortical cells in primary culture with ACTH or cyclic-AMP for 2 days results in similar increases in the volume of cells, of the mitochondrial and "membrane space" compartments and of the surface area of the smooth endoplasmic reticulum and mitochondrial cristae, and decrease in the lipid content of the cells. These changes were more marked after 8 days of treatment. Treatment for 2 days with cyclic-GMP had no striking effects on cell ultrastructure, whereas an 8-day treatment led to ultrastructural changes similar to those obtained after 2 days of ACTH- or cyclic-AMP-treatment. A discrete population of untreated cortical cells maintained a slow proliferation that was not effected by exposure to cyclic-GMP, but was significantly increased in cultures treated with ACTH or cyclic-AMP. Radioimmunological studies showed that untreated cortical cells kept secreting progesterone and cortisol and that ACTH, but neither cyclic nucleotide, increased the secretion rate per cell of both hormones. These results assign a major role to cyclic-AMP and a minor one to cyclic-GMP in the mediation of the differentiation-promoting and trophic effects, but not in the steroidogenic effects of ACTH on the human adrenal cortex.

Adrenal Cortex↗
PubMed1978

Effects of chronic treatment with ACTH on the intracellular levels of cyclic-AMP and cyclic-GMP in the rat adrenal cortex.

The effects of chronic ACTH treatment on the increase in the intracellular concentration of cyclic-AMP and cyclic-GMP acutely elicited by ACTH in the rat adrenal cortex were investigated. The results are consistent with the hypothesis that chronic ACTH treatment stimulates a) the de novo synthesis of adenylate- and guanylate-cyclase or b) the synthesis of new specific membrane receptors for ACTH.

Adrenal Cortex↗
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↗
PubMed1978

Investigations on the turnover of adrenocortical mitochondria. XII. Studies on the mechanism of the ACTH-induced elongation of the half-life of rat zona fasciculata mitochondria.

The half-life of rat adrenocortical mitochondria was determined by high resolution autoradiography and liquid scintillation spectroscopy as previously described (Mazzocchi et al., '76). The results obtained by the two approaches were in good agreement. In the normal rats the half-life of adrenocortical mitochondria averaged 11 days. ACTH significantly increased mitochondrial half-life to about 16 days, and chloramphenicol significantly decreased this parameter in both untreated and ACTH-administered rats to about seven days. It is suggested that the ACTH-induced maintenance and slowing down of the degradation rate of adrenocortical mitochondria 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. IX. A stereological study of the effects of chronic treatment with acth on the size and number of mitochondria from adult human adrenocortical cells cultured in vitro.

The effects of ACTH on the mitochondria of adult human adrenocortical cells cultured in vitro were investigated by electron microscopic and stereological methods. It was found that ACTH induces increase in the volume of the mitochondrial compartment, which is due to both a hypertrophy and an increase in number of the organelles. The hypothesis that ACTH controls the growth and proliferation of human adrenocortical mitochondria is discussed.

Adrenal Glands↗
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↗