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A Menichelli

Publications and source records attributed to A Menichelli.

41 records · Page 3Linked to original sources
PubMed1977

Cyanide insensitive oxidase in platelets of newborn infant.

The authors studied the behaviour of neonate platelet O2 consumption after the addition of pyridine nucleotide compared to adult controls. O2 consumption of neonate platelets after NADH addition was 103,2 millimicronmol O2/10(9)/hr (SE = 24,74) and in adult controls 188,8 millimicronmol O2/10(9)/hr (SE = 36,46). After the addition of NADPH O2 consumption was, respectively, 233,5 millimicronmol (SE = 46,29) and 218,3 millimicronmol (SE = 30,01).

Blood Platelets↗
PubMed1977

The effect of 2,3-diphosphoglycerate on oxygen consumption burst in thrombin-stimulated platelets.

2,3-Diphosphoglycerate (2,3-DPG) modifies platelet function; it diminishes aggregation and the release reaction. The hypothesis that this occurs through a modification of the intracellular level of cyclic AMP or through an alteration in the synthesis of prostaglandins has been proposed. Since the release reaction occurs simultaneously with a burst in the consumption of oxygen, the authors have studied the effect of 2,3-DPG on oxygen consumption after the addition of thrombin with or without the addition of substances which modify platelet metabolism (aspirin, theophylline, glucagon, etc.). It was observed that 2,3-DPG diminishes oxygen consumption induced by thrombin. This mechanism alters the platelet membrane function.

Adult↗
PubMed1976

Oxygen consumption in platelets of newborn infants before and after stimulation by thrombin.

The authors compared the oxygen consumption in platelets from the umbilical cord blood of 36 healthy newborn infants with that of 27 adult subjects, before and after thrombin addition (1.67 U/ml). Oxygen consumption at rest was 6 mumol/10(9)/min in adult control platelets and 5.26 in newborn infants. The burst in oxygen consumption after thrombin addition was 26.30 mumol/10(9)/min in adults and 24.90 in infants. Dinitrophenol did not inhibit the burst of O2 consumption in platelets in 8 out of 10 newborn infants, while the same concentration caused a decrease in 9 out of 10 adult subjects. Deoxyglucose inhibited the burst in O2 consumption in newborn infant and adult platelets by about 50%. KCN at the concentration of 10(-4) M completely inhibited basal oxygen consumption but did not completely inhibit the burst after thrombin. At the concentration of 10(-3) M, it inhibited both basal O2 consumption and the burst in infants and adult subjects.

Blood Platelets↗
PubMedDate not supplied

Superoxide release by human polymorphonuclear leukocytes in the presence of deferoxamine.

BACKGROUND AND OBJECTIVE: Anecdotal reports in patients with acute and chronic iron overload have recently indicated that the efficacy and safety of an alternative chelation program including intravenous and/or continuous delivery of deferoxamine (DFO) may be in contrast with the risk of developing lung injury. Production of oxygen radicals has been postulated to be an important mechanism by which polymorphonuclear leukocytes (PMNs) could cause tissue injury in patients undergoing this alternative treatment method. METHODS: PMNs obtained from healthy donors were incubated at 37 degrees C for 30 min with DFO (across the drug concentration 0.125 to 10 mg/mL). Superoxide (O2) production was measured by superoxide inhibitable cytochrome c reduction as well as by an NBT densitometric kinetic test. In the same run the effect of lipid peroxidation was demonstrated by means of a malonyl-dialdehyde (MDA) assay. RESULTS: Preincubation of PMNs with any study concentration of DFO significantly enhanced O2 release as well as MDA production upon PMA stimulation. Maximal intracellular and extracellular O2-release as well as MDA production occurred at certain drug concentrations. INTERPRETATION AND CONCLUSIONS: Our in vitro findings suggest that O2-release may be an additional detrimental contribution to tissue injury in some patients who develop pulmonary toxic effects while on intravenous and/or continuous DFO administration.

Antidotes↗