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At least 145 records · Page 8Linked to original sources
PubMed2005

Effects of lipopolysaccharides from gram-negative bacteria on the level of thiols in blood platelets.

Lipopolysaccharide (endotoxin, LPS) activates blood platelets and stimulates generation of free radicals in these cells. The mechanism of platelet activation induced by LPS is not known. The aim of the present study was to examine how glutathione (GSH) and other thiol-containing compounds are involved in the oxidative stress in blood platelets caused by LPS. The HPLC technique has been used on the analysis of non-protein thiols from human blood platelets treated with lipopolysaccharides of different gram-negative bacteria (Proteus mirabilis, Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa). Our results show that LPSs caused an increase (about 10%) of the level of reduced glutathione (GSH) and other nonprotein thiols such as cysteine (CSH) and cysteinylglycine (CGSH), whereas the total pool of these compounds was almost unchanged. LPS may react directly with thiols, since after incubation of LPSs with glutathione alone (in reduced form) we observed a distinct decrease of the level of platelet GSH.

Blood Platelets↗
PubMed1979

Study of the two pathways for arachidonate oxygenation in blood platelets.

During collagen-induced blood platelet aggregation, arachidonic acid is set free from membrane phospholipids and subsequently converted into 12-hydroxyeicosatetraenoic acid by arachidonate lipoxygenase and into thromboxane A2, 12-hydroxyheptadecatrienoic acid (HETE) and malondialdehyde by cyclooxygenase and thromboxane synthase. Lipoxygenase and cyclooxygenase have optimal activity at neutral to basic pH, while the thromboxane synthase is pH-independent between 5 and 9. These enzymes are membrane-bound. The cyclooxygenase is rapidly inactivated upon membrane disruption by nonionic detergents or phospholipid degradation with phospholipase A2. It was found that platelet phospholipase A2 preferentially splits off fatty acid with four double bonds. Eicosatetraynoic acid was used to investigate the physiological function of the arachidonate lipoxygenase during collagen-induced aggregation of rat blood platelets. This fatty acid is a more efficient inhibitor of lipoxygenase than of cyclooxygenase. At an inhibitor concentration of 0.6 microgram/ml, platelet aggreation, 12-hydroxyeicosatetraenoic acid production as well as 15-hydroxytryptamine release are completely inhibited, while there is an apparent stimulation of the cyclooxygenase. These results indicate that arachidonate lipoxygenase is essential for irreversible blood platelet aggregation.

Animals↗
PubMed2005

Oxidative stress in blood platelets from schizophrenic patients.

Oxidative stress in blood platelets is observed in various diseases, including neuropsychiatric disorders. The aim of our study was to evaluate oxidative stress in blood platelets from patients with schizophrenic disorders by measuring the activity of the platelet antioxidative enzyme, superoxide dismutase (SOD), concomitant with the level of thiobarbituric acid reactive species (TBARS). In blood platelets obtained from schizophrenic patients (with paranoid schizophrenia according to DSM-IV criteria) and from healthy volunteers the level of reactive oxygen species was also measured via chemiluminescence. In resting blood platelets from schizophrenic patients the chemiluminescence was higher than in platelets from control subjects (P < 0.05), but in thrombin-activated platelets an increase (about 53%) of chemiluminescence was observed, however this increase was lower than in thrombin-stimulated platelets from healthy subjects (101.5%). The results indicate that in platelets from schizophrenic patients generation of reactive oxygen species is enhanced. Moreover, we observed that SOD activity in blood platelets from schizophrenic patients was significantly lower than in control platelets and that a correlation exists between increased lipid peroxidation and inhibition of the activity of this antioxidative enzyme in schizophrenic platelets.

Adolescent↗
PubMed1982

The effect of diamide (azodicarboxylic acid-bis-dimethylamide) on sulfhydryl group content, proteins, and the location of phosphatidylethanolamine in human blood platelets.

Treatment of human blood platelets with the thiol-oxidizing agent, diamide, causes rapid oxidation of glutathione and alterations in aggregation and release reaction. Moreover, cross-linking of proteins was observed. Three high molecular weight bands of 200 - 240 X 10(3) daltons and a band of 66 X 10(3) daltons were involved in this process. After reduction with dithiotreitol the normal pattern was received. In contrast to the erythrocyte, the cross-linking of platelet proteins was not accompanied by a reorientation of phosphatidylethanolamine in the membrane. Also a considerably smaller effect of diamide on platelet protein sulfhydryl group content was measured.

Azo Compounds↗
PubMed1998

Increased histamine content in Ca2+-ionophore A23187-activated human blood platelets.

Stimulation of human blood platelets with Ca2+-ionophore A23187 at the concentrations of 0.5, 1, 2 and 3 micromol/ litre increased the total platelet histamine content from 25 ng (resting platelets) to 35, 40, 42 and 47 ng/10(8) platelets, respectively. The maximum rise was 90% , while in the presence of thrombin (0.01-1 NIH U/ml) or phorbol 12-myristate 13-acetate (PMA) (10-100 nmol/l) histamine content rose maximally by 40%. Ionophore induced a histamine increase in the same concentration range as that needed to induce platelet aggregation and liberation of [3H]-arachidonic acid. Decrease of temperature from 37 to 0 degrees C or inhibitors of platelet functions, such as acetylsalicylic acid (1 mmol/litre) or [H1]-histamine receptor antagonist Dithiaden (0.1 mmol/litre), 1 inhibited histamine liberation from A23187- stimulated platelets, but did not affect the total rise in histamine content. The presented results indicate that, similarly as with other stimuli, Ca2+-ionophore A23187 activation of human blood platelets is accompanied by histamine synthesis.

Journal Article↗
PubMed1992

Concentration and uptake of taurine in umbilical blood platelets.

The concentration and uptake of taurine in the umbilical and adult blood platelets were studied. Taurine was the most abundant free amino acid in both umbilical and adult blood platelets. The taurine concentration in umbilical blood platelets (2.30 pmoles/10(4) cells) was significantly lower than that of adult blood platelets (3.27 pmoles/10(4) cells) in contrast to the reverse relationship in taurine concentrations in umbilical and adult blood plasma. No other amino acid showed such significant difference in the concentrations between umbilical and adult blood platelets. Taurine uptake into umbilical blood platelets was temperature sensitive and sodium-dependent in a manner similar to that of adult blood platelets. The uptake conformed well to Hanes-plot. The Vmax of the uptake into adult blood platelets was about 3.6 times higher than that of umbilical blood platelets, but no significant difference was seen in the Km value between the two groups.

Amino Acids↗
PubMed1982

Comparison of the major membrane glycoproteins and proteins of human, rabbit and rat blood platelets.

Rabbit and rat blood platelets behave differently from human platelets in response to a number of aggregating agents. The aim of this work was to compare platelet membrane glycoproteins (GP) and proteins of these 3 species and relate these results to physiological functions. Washed platelets were surface labelled by techniques specific for their oligosaccharide (sialic acid, galactose/N-acetyl galactosamine) or protein moieties, and separated on a high resolution Laemmli SDS polyacrylamide gel. Higher labelling of terminal galactose/N-acetyl galactosamine residues was obtained for rat and rabbit platelets as compared to human. Glycoproteins of rabbit and rat platelets migrating at the same position as the most sialylated human platelet GP (Ib), were insignificantly labelled. However, in rabbit and rat platelets, the most sialylated GP were located at an apparent molecular weight (Mr) similar to and above human Ia, and part of this GP was lost in the supernatant in the presence of 0.002 M Ca++. Rat membrane proteins having a similar Mr to iodinated human platelet membrane proteins (IIb, IIIa) were weakly labelled in contrast to rabbit membrane proteins. These studies demonstrate differences between the platelet membrane protein and GP composition of rabbit, rat and human platelets, which may explain some of the differences observed in vitro with aggregation responses in these species.

Animals↗
PubMed1991

ADP induced blood platelet activation: a review.

Blood platelet aggregation by ADP plays a major role in the development and extension of arterial thrombosis. ADP is an original physiological agent in that, taking part as a substrate, product or allosteric effector in a large number of intracellular metabolic pathways, it also behaves as an agonist of blood platelet aggregation as do other agents including thrombin, platelet activating factor and collagen, but with probably different, yet unknown signal transduction pathways and also with unknown receptors. We discuss, in this review, how ADP induces the characteristic functional responses of platelets, namely shape change, induction and exposure of the fibrinogen binding sites on the GP IIb-IIIa complex, fibrinogen binding to its receptor and platelet aggregation, and the intracellular biochemical events underlying these functions. The present concepts of ADP receptor(s) are presented with their discrepancies. Platelet diseases related to ADP and pharmacological inhibition of ADP induced platelet aggregation are also discussed. Finally, the idea is put forward that the ADP receptor might belong to the family of G protein coupled receptors.

Adenosine Diphosphate↗
PubMed2002

[The phagocytic activity of blood platelets in different parasitic diseases].

Blood platelets take part in immune reactions of the organism, especially in anti-parasitic immunity. We conducted the phagocytic activity of blood platelets. This experiments were done on 40 patients infected with Giardia intestinalis (26), Ascaris lumbricoides (8), Entamoeba histolytica/Entamoeba dispar (6). Blood for analysis was collected thrice, before treatment (P1), after two weeks (P2), and after two months treatment with anti-parasitic drugs (P3). Control group consisted of 32 healthy people. The evaluation of platelet phagocytic activity revealed that the mean percentage of phagocytizing platelets in patients was 2.87 (P1), 2.94 (P2), 2.86 (P3), being significantly lower in controls (mean 2.15), the difference was statistically significant (p < 0.05). No statistically significant difference was found in the mean phagocytic index between patients (P1, P2, P3) and controls. Our general conclusion is--parasites are able to stimulate phagocytic activity of blood platelets.

Adult↗
PubMed2000

Activation of blood platelets after percutaneous transluminal coronary angioplasty and coronary artery bypass graft surgery.

We have evaluated the activation of platelets in blood samples taken from patients with stable angina undergoing balloon angioplasty (percutaneous transluminal coronary angioplasty [PTCA]) (n=11) or coronary artery bypass grafting (CABG) under hypothermic (n=11) or normothermic conditions (n=11). We have found that surface expression of P-selectin on platelets in whole blood from PTCA patients upon thrombin treatment was significantly reduced, as compared with control platelets from healthy subjects. This effect was partially reversed when platelets washed from the same blood sample were used, but even then P-selectin expression was significantly lower in PTCA patients than it was in control subjects. There was a significant increase in basal expression of P-selectin in blood platelets taken from patients who underwent CABG under normothermic conditions (warm blood cardioplegia) as opposed to hypothermic patients (cold crystalloid cardioplegia). These platelets retain the ability to respond to agonists, although to a much lower extent than do those from healthy control donors. The surface exposure of P-selectin on resting and thrombin-treated platelets isolated from CABG surgery patients was not different from that of the control platelets. The adhesion to fibrinogen of resting and thrombin-treated platelets from patients who underwent balloon angioplasty as well as CABG surgery under normothermic and hypothermic conditions was significantly reduced when compared with the fibrinogen of the control platelets. These results suggest that the function of platelet fibrinogen receptor is impaired in patients with stable angina pectoris and that PTCA and CABG surgery activates platelets.

Adult↗