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S Macaione

Publications and source records attributed to S Macaione.

At least 19 recordsLinked to original sources
PubMed1999

Changes in plasma, erythrocyte, and platelet magnesium levels in normotensive and hypertensive obese subjects during oral glucose tolerance test.

We evaluated the 75-g oral glucose tolerance test (OGTT)-induced modifications in glucose, insulin, and norepinephrine plasma concentrations, and in plasma, erythrocyte, and platelet magnesium levels in two groups of obese subjects (normotensive obese, NT-Ob, N = 19; hypertensive obese, HT-Ob, N = 15), and in a group of healthy control subjects (N = 12). During OGTT we detected a reduction in plasma magnesium concentrations and an increase in erythrocyte and platelet magnesium levels in the controls, whereas in both normotensive and hypertensive obese subjects, there was a reduction in plasma, erythrocyte, and platelet magnesium levels. Furthermore, no statistically significant difference was detected among the groups studied as regards delta-plasma magnesium. On the other hand, delta-erythrocyte magnesium and delta-platelet magnesium were negative in the NT-Ob (delta-erythrocyte magnesium: -0.24+/-0.08 mmol/L; delta-platelet magnesium: -0.49+/-0.09 micromol/10(8) cells) and HT-Ob (delta-erythrocyte magnesium: -0.20+/-0.10 mmol/L; delta-platelet magnesium: -0.50+/-0.11 micromol/10(8) cells) groups, and positive in control subjects (delta-erythrocyte magnesium: 0.40+/-0.08 micromol/L; delta-platelet magnesium: 0.47+/-0.09 mmol/ 10(8) cells). Finally, a direct correlation was found between delta-norepinephrine and delta-erythrocyte magnesium (r = 0.80, P < .01) in the control group, and a negative correlation was detected between delta-norepinephrine and delta-platelet magnesium (r = -0.58, P < .05) in the HT-Ob group. Our results seem to indicate that the insulin resistance status, the hyperglycemia, and the disregulation of the adrenergic system in obese subjects could be involved in the pathogenesis of the magnesium homeostasis impairment observed in the obese subjects.

Adult↗
PubMed1999

Intracellular polyamine levels are involved in NMDA-evoked nitric oxide production in chick retina cells.

The NMDA-sensitive glutamate receptor complex can be modulated by numerous drugs and endogenous substances such as polyamines. We studied the pathway of arginine/nitric oxide/cyclic GMP in cultured chick retina cells through NMDA receptor activation, seen as a function of both differentiation stages of culture and intracellular polyamine levels. In our experimental conditions, the nitric oxide synthase activity was stimulated by NMDA from three to four times between embryonic day (E) 8 plus 5 days in vitro (C) and E8C7. The NMDA response was blocked by MK-801 (10 microM) by >60% at stage E8C5. During culture differentiation, the NMDA-induced increase in nitric oxide synthase activity at the E8C5 stage was blocked by preliminary incubation (24 h) of the cells with alpha-difluoromethylornithine, the inhibitor of polyamine biosynthesis. This effect was assessed by a reduction of NMDA-evoked cyclic GMP formation in polyamine-depleted retina cells. Thus, intracellular polyamine levels are involved in NMDA-evoked nitric oxide production. Our results indicate that (a) the developmental pattern of polyamine levels can be associated with the modulation of NMDA-evoked events and (b) the NMDA-mediated effects have been reduced in alpha-difluoromethylornithine-treated cell cultures. These observations provide evidence for a physiological interaction between polyamines and NMDA-sensitive glutamate receptors during differentiation stages of cultured chick retina cells.

Animals↗
PubMed1998

Plasma (total and ionized), erythrocyte and platelet magnesium levels in renal transplant recipients during cyclosporine and/or azathioprine treatment.

We evaluated total and ionized plasma magnesium levels, and erythrocyte and platelet magnesium concentrations from two groups of renal transplant recipients treated either with cyclosporine, azathioprine and prednisolone (group CAP, n = 8) or with azathioprine and prednisolone (group AP, n = 13), and in a group of age- and sex-matched healthy subjects (n = 10). Reduced plasma (total and ionized), erythrocyte and platelet magnesium concentrations were found in both CAP and AP groups with respect to controls (CAP: total plasma Mg median 0.61 vs 0.86 mmol/L, p < 0.01, ionized plasma Mg median 0.43 vs 0.58 mmol/L, p < 0.001, erythrocyte Mg median 2.18 vs 2.56 mmol/L, p < 0.05, platelet Mg median 1.75 vs 2.84 mmol/10(8) cells, p < 0.001; AP: total plasma Mg median 0.62 vs 0.86 mmol/L, p < 0.01, ionized plasma Mg median 0.48 vs 0.58 mmol/L, p < 0.001, erythrocyte Mg median 2.30 vs 2.56 mmol/L, p < 0.05, platelet Mg median 1.75 vs 2.84 mumol/10(8) cells, p < 0.001), while no difference was found between the two groups of transplant recipients as regards plasma and intracellular magnesium levels. Magnesium fractional excretion was higher in transplant recipients than in the control group (Mg fractional excretion median AP 18.6 per cent and CAP 12.8 per cent vs controls 3.5 per cent), whereas no difference was found between patients and control subjects for urinary magnesium 24h excretion. Moreover, in the whole group of transplant recipients (n = 21), urinary magnesium showed an inverse correlation with platelet (rs = -0.54, p < 0.05) and ionized plasma magnesium (rs = -0.48, p < 0.05), and time after transplantation showed a negative correlation with platelet magnesium concentrations (rs = -0.73, p < 0.001), and a direct correlation with fractional magnesium excretion (rs = 0.53, p < 0.05). Finally, a direct relationship between platelet magnesium and ionized plasma magnesium was also detected in the whole group of transplant recipients (rs = 0.47, p < 0.05). Both intraplatelet magnesium depletion and ionized plasma magnesium reduction induced by immunosuppressive therapy could be involved in the increased risk from atherosclerotic disease in renal transplant recipients.

Arteriosclerosis↗
PubMed1998

[Obesity and hypertension: the role of magnesium].

We focus on the recent "ionic hypothesis", in which an alteration of ionic metabolism represents a peculiar event in the pathogenesis of obesity and hypertension. We report the results from our original studies in which we evaluated intraplatelet magnesium levels. In a study on normotensive and hypertensive patients with non insulin-dependent diabetes mellitus and healthy control subjects, we showed a common reduction of plasma, erythrocyte and platelet magnesium levels in both normotensive and hypertensive diabetics with respect to control. Anyway, hypertensive diabetics showed a greater reduction of intraplatelet magnesium concentrations when compared to normotensive diabetics. Using the same technique, we found reduced erythrocyte and platelet magnesium concentrations in patients with essential hypertension with respect to the control group. In a successive study, we found, in the group of normotensive obese, that erythrocyte and platelet magnesium levels were significantly lower than those of the control group, while in hypertensive obese patients a reduction of plasma magnesium levels has been also detected. In conclusion, in these studies has been confirmed the existence of a reduction of the intracellular magnesium concentrations, which is common in hypertensive and obese patients.

Blood Platelets↗
PubMed1997

Nitric oxide mediates NMDA-evoked [3H]GABA release from chick retina cells.

The stimulation of NMDA receptor increased [3H]GABA release from preloaded cultured retina cells. This effect appears to be mediated by NO production, since addition of L-NA reduces NMDA-evoked [3H]GABA release. Spermine/NO complex, an NO donor, mimics the effect produced by NMDA. The addition of zaprinast, a phosphodiesterase inhibitor, as well as 8-Br-cGMP enhances the NMDA-evoked [3H]GABA release. These results agree with the existence in chick retina cells of NO/cGMP pathways and support a role for NO in NMDA-evoked events. The activation of this receptor complex through maturative stages of the retina together with the NO-mediated increase in GABA release may account for NMDA differentiative effect in culturing retina cells.

1-Methyl-3-isobutylxanthine↗
PubMed1997

beta-Endorphin enhances polyamine transport in human lymphocytes.

Opioid peptides, such as beta-endorphin (beta-end), are capable of modulating in vitro proliferative response of lymphocytes. We attempted to determine the role of extracellular polyamines in the regulation of immune responses to opioid peptides by measuring the extent of polyamine uptake as adaptional response to cell activation. beta-end dose-dependently enhanced the incorporation of radioactive spermidine and spermine. When the cells were depleted of spermidine, with addition of specific inhibitors of both biosynthesis and interconversion pathway, a large increase in the incorporation of radioactive spermidine was observed. This effect appeares to be specific for beta-end, although a non-opiate-specific receptor could be involved, since beta-end-enhanced incorporation of radioactive spermidine is not blocked by naloxone. We conclude that the enhancement of polyamine incorporation may be considered as an integral component of lymphocyte activation by beta-end.

Adrenocorticotropic Hormone↗
PubMed1996

Nitric oxide enhances amino acid release from immature chick embryo retina.

Nitric oxide (NO) was investigated for its ability to induce amino acid release from immature chick retina. The production of endogenous NO by activation of NO synthase after stimulation of N-methyl-D-aspartate (NMDA) subtype of glutamate receptor caused a significant increase in basal release of gamma-aminobutyric acid (GABA) and glutamine, whereas a more modest increase in the glutamate release was also observed. The exposure of chick retina from 9-day-old embryos to NO-generating compounds, S-nitroso-N-acetylpe-nicillamine (SNAP) and sodium nitroprusside (SNP) produced a dose dependent increase in GABA, glutamine, and glutamate release. This effect was reduced by about 80% by haemoglobin. These results indicate that NO has a stimulatory effect on amino acid release from chick embryo immature retina. However, this effect does not appear to involve a cGMP-related mechanism because 8-bromo-cGMP, a stable analogue of cGMP, failed to affect spontaneous amino acid release and because zaprinast did not enhance NMDA-stimulated release. In conclusion, our present observations may account for a role of NMDA-mediated events in the biochemical maturation under depolarizing conditions.

Amino Acids↗
PubMed1996

Nitric oxide synthase in chick embryo retina during development.

High levels of nitric oxide synthase were found in the early stages of developing chick embryo retina. The enzyme activity sharply decreased up to 13-day-old chick embryo retina, when the level of the last embryonic day was reached. The results show that nitric oxide is synthesized in chick embryo retina prior to synaptogenesis. The incubation of chick embryo retinas in presence of NMDA increased the synthesis of nitric oxide, thus, the appearance of nitric oxide production before the synaptogenesis in the retina as well as in the brain may be considered as signal for the development and shaping of neuronal and non-neuronal cells.

Animals↗
PubMed1992

Polyamines are involved in retinoic acid-mediated induction of tissue transglutaminase in human peripheral blood monocytes.

The differentiation of human peripheral blood monocytes (HPBM) into macrophages, when cultured in vitro, has been associated with an increase in the expression of tissue transglutaminase (TGc). Retinoic acid (RA) addition to 5-day-old cultured monocytes, 36 h later induced about 5-folds increase of TGc content. The preliminary exposure of cultured monocytes to alpha-difluoromethylornithine (DFMO) significantly reduced TGc induction caused by RA. DFMO alone does not induce significant changes in the time-course of TGc activity. In cultured monocytes exposed to DFMO, putrescine and spermidine, but not spermine were significantly depleted. The supplementation of putrescine (1 mM) or spermidine (0.5 mM) to culture medium reversed the inhibiting effect of DFMO on RA-mediated induction of TGc. However, the addition of polyamines in the absence of RA or DFMO did not mimic the induction of TGc by RA. We conclude that TGc induction by RA during in vitro maturation of monocytes to macrophages may be modulated by polyamine availability.

Cell Differentiation↗
PubMed1988

Glucocorticoid regulation of spermidine acetylation in the rat brain.

The effect of glucocorticoids on polyamine metabolism has been elucidated further by measuring putrescine, spermidine, and spermine levels as well as ornithine decarboxylase, S-adenosylmethionine decarboxylase, and N1-acetylspermidine transferase activities in the hippocampus, cerebellar cortex, vermis, and deep nuclei of adrenalectomized rats. At 6 h after corticosterone or dexamethasone administration, the specific activities of ornithine decarboxylase and N1-acetylspermidine transferase showed the greatest increases in all brain tissues examined, and at 12 h, S-adenosylmethionine decarboxylase activity was not increased significantly. The hippocampus and cerebellar regions displayed different responses to corticosterone and dexamethasone, corresponding to the distribution of glucocorticoid and mineralocorticoid receptors. Corticosterone and dexamethasone increased ornithine decarboxylase and N1-acetylspermidine transferase activities in a dose-dependent manner, with dexamethasone being more active than corticosterone in all tissues. However, estradiol, progesterone, testosterone, and aldosterone were only active at doses greater than 5 mg/kg. The great increases in ornithine decarboxylase and N1-acetylspermidine transferase activities were accompanied by a marked increase in putrescine level and a small decrease in spermidine level. Our data confirm that the hippocampus and cerebellum are glucocorticoid target tissues and suggest that the increase in the content of putrescine, following acute treatment with glucocorticoids, is dependent on ornithine decarboxylase as well as N1-acetylspermidine transferase induction.

Acetylation↗
PubMed1986

Polyamine localization and biosynthesis in chemically fractionated rat retina.

For elucidation of polyamine localization and biosynthesis in various cell types of rat retina, the putrescine, spermidine, and spermine contents as well as the ornithine decarboxylase and S-adenosylmethionine decarboxylase activities have been measured in retinal cell layers obtained by the selective cytotoxic action of iodoacetate on photoreceptor cells and of monosodium glutamate on higher-order retinal neurons. A notable depletion only in spermine content was associated with loss of the visual cell layer. Total ornithine decarboxylase and S-adenosylmethionine decarboxylase activities per retina were significantly lower in all chemically fractionated tissue, but loss of the photoreceptor layer produced the greatest decrease. The specific activities of these enzymes did not show marked changes in rat retinas deprived of inner neurons. The data support the suggestions that polyamine synthesis, storage, and catabolism have different distributions in the retinal layers and that the spermine levels and the high value of the spermine/spermidine molar ratio might depend essentially on the proportion of rods to cones.

Adenosylmethionine Decarboxylase↗
PubMed1985

Effect of intraventricular putrescine on adenosylmethionine decarboxylase in rat hypothalamus and caudate nucleus.

Effects of intracerebroventricularly injected putrescine on adenosylmethionine decarboxylase activity in rat hypothalamus and caudate nucleus were studied. Doses that lacked the capacity to produce behavioral and electrocortical epileptogenic disorder caused a significant activation of enzyme occurring between 10 and 15 min after injection. The changes in hypothalamic and caudate nucleus enzyme activity after putrescine administration were dose-dependent, and they supported the assumption that limiting putrescine concentration in vivo may play a role in adenosylmethionine decarboxylase regulation.

Adenosylmethionine Decarboxylase↗
PubMed1984

Phenolic and tyrosyl ring deiodination in thyroxine from rat retina during postnatal development.

To elucidate tetraiodothyronine (T4) metabolism in developing rat retina 5-monodeiodinating and 5'-monodeiodinating activities were studied. T4 was incubated with aliquots of homogenate or crude primary subcellular fractions, and the 3,3',5'-triiodothyronine (rT3) or 3,5,3'-triiodothyronine (T3) produced were measured by radioimmunoassay. Reaction rates were dependent on incubation time, tissue amount, temperature and pH. The optimum pH values were 7.8 and 7.2 respectively for rT3-forming and T3-forming systems. Conversion of T4 to either T3 or rT3 was dependent on dithiothreitol concentration, and the T4-5'-deiodinating activity was inhibited by propylthiouracil. Deiodinase activities were mainly found in the crude microsomes. The retinal 5'-monodeiodination rate of T4 was immeasurably low by the 2nd day and the highest values were reached on 15th day of postnatal development. On the other hand deiodination of the T4 tyrosyl ring shows a progressive decline from birth, and adult values were reached on the 15th day. Data support the hypothesis that, in developing rat thyroxine, phenolic and tyrosyl-ring deiodinase activities are present in the retina and their reciprocal changes may regulate morphological and biochemical cell maturation.

Animals↗
PubMed1984

Retina maturation following administration of thyroxine in developing rats: effects on polyamine metabolism and glutamate decarboxylase.

The effects of subcutaneous daily treatment with thyroxine on cell proliferation, differentiation, polyamines, and gamma-aminobutyric acid metabolism in the rat retina were studied during the first 20 postnatal days. The retinal layers of the treated rats displayed an enhanced cell differentiation which reached its maximum 9-12 days from birth; but this effect stopped very quickly and was finished by the 20th postnatal day. Primarily there was an increase in ornithine decarboxylase activity which was accompanied by an increase in putrescine, spermidine, and spermine levels. S-Adenosylmethionine decarboxylase was induced later than ODC; corresponding with the enhanced synaptogenesis, glutamate decarboxylase increased 15-fold between the fourth and 15th days. Our data are consistent with the hypothesis that thyroxine may exert some of its effects by inducing the enzymes which regulate polyamine metabolism and synaptogenesis.

Adenosylmethionine Decarboxylase↗
PubMed1983

Effects of thyroxine on methionine adenosyltransferase activity in rat cerebral cortex and cerebellum during postnatal development.

Methionine adenosyltransferase (MAT) activity was evaluated in cerebral cortex and cerebellum in controls and in rats treated with thyroxine. In controls the enzyme showed a different pattern in cerebral cortex and cerebellum during neonatal and late suckling periods. Hyperthyroid rats showed a significant increase of the enzyme in cerebral cortex only at the 2nd day of the neonatal period; in cerebellum the developmental pattern of MAT in neonatal period was anticipated temporally by 2-4 days. During the late suckling period thyroxine treatment produced in cerebellum a significant decrease in MAT activity at the 15th day after birth. From these data, we propose that hyperthyroidism may cause precocious induction of MAT both in cerebral cortex and in cerebellum and that the increased availability of S-adenosyl-L-methionine during the neonatal period could be related to its utilization also in polyamine biosynthesis.

Animals↗
PubMed1982

S-adenosylmethionine decarboxylase levels in rat retina during postnatal development.

S-Adenosylmethionine decarboxylase from rat retina is similar to that isolated from other rat tissues with regard to kinetic parameters, pH optimum, putrescine requirement, and sensitivity to spermine. The enzymic activity increases during the first 7 days of postnatal life but decreases until the 20th day. After this period AdoMet decarboxylase activity increases, to reach the highest values at the 90th day. This behavior suggests that such enzymic activity is responsible for spermidine and spermine levels in rat retina and that a high content of retinal spermine might have a role in the photoreceptor outer segment renewal.

Adenosylmethionine Decarboxylase↗
PubMed1980

Effects of intraventricular gamma-acetylenic-GABA on GABA concentrations, GABA-T and GAD in several areas of the chick brain.

The great interest in new compounds able to increase GABA concentration in the brain as potential antiepileptic drugs has led to the synthesis of powerful inhibitors of GABA transaminase (GABA-T) e.g. gamma-acetylenic GABA (GAG) and gamma-vinyl-GABA. Present experiments were aimed to study behavioral, electrocortical and biochemical effects of GAG after its intraventricular injection. It has been shown that in chicks the microinjection of GAG into the third cerebral ventricle produced a biphasic behavioral and electrocortical syndrome : an initial phase of behavioral and electrocortical sleep followed by a paradoxycal increase in motor activity and a very intense behavioral and ECoG arousal pattern. In addition intraventricular GAG (0.8 mumol) produced a significant increase 1 and 2 h later in GABA concentration in the diencephalon and brain-stem whereas no changes occurred in other brain areas e.g. cerebral hemispheres, optic lobes. Higher doses (1.6 mumol), produced after 1 h, concomitantly to the increased GABA concentration, a significant GABA-T inhibition and a profound inhibition of glutamate-decarboxylase in the diencephalon and brain-stem. Present experiments may explain the paradoxical behavioral, motor and electrocortical stimulation observed at the time of GABA increase concentration and suggest that a small functional neuronal pool of GABA, more than the whole absolute levels of GABA in a given area of the brain, seems to be involved in the control of GABAergic mediated inhibitory mechanisms.

4-Aminobutyrate Transaminase↗