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D Del Principe

Publications and source records attributed to D Del Principe.

At least 37 records · Page 2Linked to original sources
PubMed1991

Hydrogen peroxide is an intermediate in the platelet activation cascade triggered by collagen, but not by thrombin.

Human blood platelets produce oxidant species when stimulated by collagen and thrombin. The oxidative burst of platelets has been studied by cytofluorimetry taking advantage of the fluorogenic dye DCFH2-DA, which is taken up and deacetylated by platelets and then oxidized to the fluorescent derivative DCF. The oxidation of DCFH2 is induced by stimulation with collagen but not with thrombin and inhibited by external catalase. Catalase also inhibited the aggregation induced by collagen, but not that induced by thrombin. Aspirin and indomethacin inhibited the formation of the fluorochrome only when platelets were stimulated by thrombin. Externally added H2O2 increased the cytoplasmic calcium content as probed by the fluorescence of Indo-1. The present data suggest that collagen induces the production of H2O2, which in turn may stimulate the aggregation of platelets through a calcium mobilization. Instead the stimulation by thrombin does not require the intermediacy of H2O2.

Aspirin↗
PubMed1991

Enhancement by growth hormone of phorbol diester-stimulated respiratory burst in human polymorphonuclear leukocytes.

The oxidative metabolic burst of mononuclear and polymorphonuclear phagocytes can be stimulated to produce free oxygen radicals. Several substances can enhance this respiratory burst activity by a priming action: recently growth hormone (rat and porcine) was demonstrated to act as a priming agent on rat peritoneal and on porcine alveolar macrophages. In our study we wanted to verify whether also human GH had a similar priming action on homologous cells, in particular on polymorphonuclear leukocytes. To determine the oxidative activity of polymorphonuclear leukocytes, after stimulation with phorbol myristate acetate, a flow-cytometric assay was employed which registered the intracellular formation of highly fluorescent products as indicators for the intracellular formation of hydrogen peroxide. The incubation of phorbol myristate acetate-stimulated polymorphonuclear leukocytes with GH resulted in a time-dependent and dose-dependent increase in fluorescence, thus demonstrating that human GH enhances in vitro the oxidative metabolic burst of these cells. The action of GH appeared to be significant after 30 min of incubation, was maximal at 60 min, and decreased after 90 min. After one hour of incubation, the first significant variation of fluorescence appeared with GH at a concentration of 50 micrograms/l. The maximum effect was seen at 100 micrograms/l with no further increase. Specificity of GH action was demonstrated by the inhibition of its effect by the addition of monoclonal antibodies to GH.

Adult↗
PubMed1990

Stimulated platelets release factor(s) affecting the in vitro response of human polymorphonuclear cells.

The metabolic and functional responses of human polymorphonuclear cells (PMNs) to thrombin-activated platelet supernatants were studied. The incubation of PMNs with supernatants from stimulated platelets (SPS) caused a 50% decrease in both killing of Staphylococcus aureus and luminol-enhanced chemiluminescence (CL) by PMNs stimulated by opsonized-zymosan (OZ), Concanavalin A (Con A), or calcium ionophore A23187. The levels of PMN intracellular fluorescence measured by flow cytometry, using the fluorochrome dichlorofluorescein diacetate (DCF-DA), were considerably less in the presence of SPS than in resting platelet supernatants (RPS). No influence of platelet supernatant on O2 consumption and O2- generation by OZ-activated PMNs was observed. The incubation of PMNs with SPS caused a significant increase in the rate of chemotaxis and aggregation elicited by Con A, OZ, and phorbol myristate acetate (PMA). The supernatant from resting platelets did not show any of the above-reported effects. Platelets previously degranulated by thrombin were unable to inhibit CL when activated with agonists. Studies on the differential release of the granules by platelets showed that the CL-quenching activity paralleled the discharge of lysosomal content. The release of myeloperoxidase (MPO) from PMNs elicited by OZ was reduced in the presence of SPS. The platelet supernatant did not affect the MPO activity if PMNs were lysed with Triton X-100. The leakage of lactate dehydrogenase (LDH) from platelets was less than 3%, and no catalase or superoxide dismutase was released. This activity withstood lyophilization, but was destroyed by 10 min heating at 100 degrees C or by treatment with proteolytic enzymes.

Blood Platelets↗
PubMed1989

Platelet lipid peroxidation in haemodialysis patients: effects of vitamin E supplementation.

In haemodialysis patients, increased concentrations of malonyldialdehyde and decreased vitamin E content indicate lipid peroxidation in the platelets from oxidative damage. The same process has been described in red blood cells and in mononuclear cells in peripheral blood. However, platelet aggregation is within normal limits and does not change after treatment with vitamin E. On the other hand vitamin E supplementation reverts completely the biochemical abnormality of the platelets.

Blood Platelets↗
PubMed1988

Treatment of acute idiopathic thrombocytopenic purpura (AITP): cooperative Italian study group results.

A cooperative Italian study group on acute idiopathic thrombocytopenic purpura (AITP) has been designed to evaluate efficacy and safety of no treatment at the onset of the disease and sequential treatment with immunoglobulin and high dose steroid. One hundred thirty-eight patients with AITP entered in the trial. Eleven patients were treated before the end of the waiting period because of bleeding. One hundred twenty-seven (92%) received no treatment for the first 10 days of the disease, 65 patients (51.18%) recovered spontaneously, 62 patients were treated with immunoglobulin, and 52 (83.8%) of them responded positively but only 36 (58.06%) permanently. There was no statistical difference between the results obtained with 400 mg/kg for 5 days versus 200 mg/kg. Twenty-four patients were treated with high doses of steroids, 20 (83.3%) with positive response, and 10 (41.66%) were permanently cured. Four (3.14%) of the patients enrolled in the protocol still had active disease at the end of treatment, and 10 relapsed within 4 months after the end of the treatment.

Adolescent↗
PubMed1986

A surface NAD-glycohydrolase of human platelets may influence their aggregation.

Human platelets may hydrolyze externally added NAD+ yielding ADPR and nicotinamide. The extent of hydrolysis is significantly higher when the platelets are stimulated. The presence of external NAD+ strongly inhibits the aggregation induced by every agonist used. It seems that adenosine or ADPR itself generated by NAD+ hydrolysis may be responsible for the inhibition of aggregation. Evidence is given that some of the NAD+ hydrolysis product is taken up by stimulated platelets.

Adenosine↗
PubMed1986

Vitamin E consumption by human blood platelets activated by latex particles.

Human blood platelet activation elicited by latex particles is associated to a 30% decrease in the cellular content of vitamin E. The vitamin E consumption is inhibited by the addition of catalase (500 U/ml) and azide (1 mM), but it is not affected by potassium cyanide (1 mM). It may be proposed that the challenge of platelets with particulate stimuli causes generation of oxygen reduction products, which leads to vitamin E depletion.

Azides↗
PubMed1985

Isotachophoresis as a useful tool for monitoring neurological complications of acute leukaemia in children.

Cerebrospinal fluid proteins from 42 children with acute lymphoblastic leukaemia were analysed by isotachophoresis. The isotachopherograms of cerebrospinal fluid taken from patients undergoing central nervous system prophylaxis with neurological complications showed an increase of several peaks (albumin, prealbumin, and an unidentified peak), and changes in the globulin zone, compared with those from patients who had completed central nervous system prophylaxis for at least six months. The most striking finding was that these alterations were not associated with any other biochemical changes in the cerebrospinal fluid, as assayed by routine analysis. Isotachophoresis may be useful in the monitoring of therapy in children affected with acute lymphoblastic leukaemia.

Brain Diseases↗
PubMed1985

Hydrogen peroxide has a role in the aggregation of human platelets.

The aggregation of platelets induced by soluble and particulate stimuli is enhanced by the addition of minute amounts of H2O2. Externally added catalase strongly inhibits the aggregation induced by particulate stimuli and by phorbol myristate acetate (PMA). The addition of aminotriazole to stimulated platelets causes a significant inhibition of intracellular catalase. This indicates the formation of H2O2 inside the platelets during activation. No effects were observed when the platelets were stimulated by the ionophore A23187.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1985

Ventricular thrombosis during permanent endocardial pacing in a pediatric patient with hemorrheological disorders.

Thrombosis in the right atrium or ventricle is a rare complication of permanent endocardial pacing in adults. To the best of our knowledge, this complication has not been previously reported at all in the pediatric age group. We report on a case of a 7-year-old boy who had large left ventricular thrombi that occurred during permanent endocardial electrical stimulation. Subsequent pulmonary emboli complicated congestive heart failure in this patient. As a diagnostic approach, echocardiography and pulmonary perfusion scintigraphy were used. We comment on possible causes of this serious complication and suggest hemorrheological and platelet activation studies in patients with permanent endocardial pacing.

Bradycardia↗
PubMed1985

Photodynamic damage induced by bilirubin on human platelets: possible relevance to newborn pathology.

Several reports have appeared showing the possibility of bilirubin-sensitized photodamage. We have extended these observations to platelets. In the presence of 300 microM bilirubin the in vitro irradiation of isolated platelets or platelet-rich plasmas with visible light induced significant lysis as determined by the release of lactate dehydrogenase (LDH). The extent of LDH release was a function of irradiation time, being about 20% after 2 h of irradiation. A loss membrane-bound ATPase activity was also observed at earlier times, indicating that membrane damage was preliminary to the lytic effect. The release of beta-thromboglobulin, induced by close cell-to-cell contact, was lower in bilirubin- and light-treated platelets with respect to controls. Our results suggest that bilirubin may act as a photodynamic agent producing some damage on human blood platelets.

Adenosine Triphosphatases↗
PubMed1984

Interaction of terbium with human platelets.

The effect of terbium on platelets has been studied by aggregation experiments and by fluorescence measurements. TbCl3 does not substitute for CaCl2 in the aggregation of platelets induced by ADP, but it may even inhibit, probably by a competition mechanism. It was impossible to observe a sensitized emission of Tb3+ in the presence of platelets. Instead the lanthanide, like Ca2+, significantly increases the aggregation of platelets induced by A23187. The fluorescence yield of this compound is greater in the presence of platelets than in buffer alone. Energy transfer appears to take place from the aromatic amino acids of the platelet membrane to the bound ionophore.

Adenosine Triphosphate↗
PubMed1984

Intravenous pulse methylprednisolone in chronic idiopathic thrombocytopenia.

Two children with chronic idiopathic thrombocytopenic purpura unresponsive to either standard corticosteroid treatment or high dose intravenous gammaglobulin, or both, were treated with intravenous methylprednisolone (15 mg/kg/day) given in pulses over three consecutive days. Both children showed a positive response and are still in remission after three months.

Child↗
PubMed1983

Opsonized-zymosan induces a respiratory burst in human blood platelets.

Opsonized-zymosan-stimulated polymorphonuclear cells show a cyanide-insensitive oxygen consumption. We have investigated whether opsonized-zymosan could induce similar metabolic change in human blood platelets. Preparation of intact human blood platelets, obtained by separation through a Ficoll layer (23% w/v) were challenged with opsonized-zymosan. The polymorphonuclear cell contamination was less than 1/10(8) platelets. The opsonized-zymosan-stimulated platelets showed an increase of oxygen consumption. The mean of oxygen burst measured by a polarographic method with a Clark electrode was 11 nmole/10(9) platelets/min (S.E.M. 4; n = 15). The duration of the burst was 2 min. Unstimulated platelets did not show the oxygen burst. The inhibitors of respiratory chain and prostaglandin synthesis completely abolished the oxygen consumption by opsonized-zymosan-stimulated platelets. The simultaneous addition of NADH (1 mM) and opsonized-zymosan induced a burst of oxygen consumption, which occurred after a variable lag phase (10-12 min) from the stimulation, also in the presence of inhibitors. This burst, which lasted about 1 min, amounted to 10 nmole/10(9) platelets/min (S.E.M. 2; n = 15) and it was higher in the presence of NAN3, a catalase inhibitor. Zymosan treated with hydrazine or heated plasma (56 degrees C) did not cause increased oxygen consumption. Inulin or inulin-treated serum did not stimulate platelets. In these experimental conditions some NADH disappeared, as shown by isotachophoresis. The results demonstrated that an immunological stimulus may activate a membrane-linked cyanide-insensitive oxygen metabolizing system.

Blood Platelets↗
PubMed1982

Hydrogen peroxide release from human blood platelets.

The release of hydrogen peroxide from human blood platelets after stimulation with particulate membrane-perturbing agents has been determined by fluorescence using scopoletin as the detecting agent. Platelet suspensions containing less than 1 polymorphonuclear leukocyte/10(8) platelets showed a significant release of hydrogen peroxide (6.11 nmol/10(9) platelets per 20 min, S.D., 0.26, n = 9) after addition of zymosan or latex particles, compared to unstimulated platelets. The release of hydrogen peroxide was only observed when the scopoletin was added to the platelet suspensions during the stimulation. Any attempt to determine hydrogen peroxide release in the supernatant at the end of the incubation with zymosan or latex failed. A NADH-dependent production of hydrogen peroxide was observed by measuring the difference of oxygen uptake in the presence and absence of catalase (500 units), which was not inhibited by potassium cyanide (1 mM). By this method the NADH-dependent cyanide-insensitive peroxide production and release was 6.0 nmol/10(9) platelets per 20 min from resting platelets (S.D., 2, n = 6) vs 15 nmol/10(9) platelets per 20 min from stimulated platelets (S.D., 2, n = 6).

Blood Platelets↗
PubMed1982

Superoxide-dependent chemotactic activity for PMNs derived from opsonized zymosan-stimulated human platelets.

Previous studies have shown that platelets exhibit a H2O2 producing, NADH-dependent system that is activated by interaction with particulate material. Current evidence suggests that this system could be critically involved in th generation of chemotactic factor(s). In the present studies, chemotactic activity for polymorphonuclear leukocytes of supernatants derived from zymosan-stimulated human platelets has been evaluated using an agarose gel technique. Supernatants of opsonized zymosan-stimulated platelets showed significant chemotactic activity (migration index = 300 +/- 50), in comparison with supernatants prepared from platelet suspensions stimulated with nonopsonized-zymosan (migration index = 10 +/- 15) or resting platelet supernatants (migration index = 15 +/- 15). Furthermore, a marked increase in chemotactic activity of the opsonized zymosan-treated platelet supernatants was demonstrated after the addition of NADH (migration index = 525 +/- 100). The inclusion of specific inhibitors of the cycloxygenase and lipoxygenase pathways resulted in a marked reduction of chemotactic activity, which was restored in the presence of NADH. Further, the addition of superoxide dismutase completely abolished the chemotactic response induced by NADH. These data suggest that platelets are the source of chemotactic factor(s) derived from the activation of a superoxide generating system.

Blood Platelets↗