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

Principe, Domenico Del; Menichelli, A; Matteis, W. De; Giulio, Stefano Di; Giordani, M.; Savini, Isabella; Agró, Alessandro Finazzi

doi:10.1016/0049-3848(91)90010-t

Cited by 63 publications

(30 citation statements)

References 18 publications

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“…Oxidative stress can be caused by as well as lead to abnormal neurotransmitter metabolism. Blood platelets, like other circulating blood cells, can also produce different ROS [25][26][27]. General sources of reactive oxygen species in blood platelets is arachidonic acid metabolism (via cyclooxygenase or 12-lipoxygenase) and the glutathione cycle [28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress in blood platelets from schizophrenic patients

2005

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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.

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Section: Discussionmentioning

confidence: 99%

Oxidative stress in blood platelets from schizophrenic patients

2005

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“…In vivo, reactive oxygen species are formed by polymorphonuclear cells, but in our isolated system they may be formed by platelets. When stimulated by agonists, human platelets are known to produce oxidant species including H 2 O 2 (50). In human platelets, low concentrations of H 2 O 2 are continuously produced with a significant rise in the concentration upon stimulation (51).…”

Section: Discussionmentioning

confidence: 99%

Decreased platelet inhibition by nitric oxide in two brothers with a history of arterial thrombosis.

Freedman

Loscalzo²,

Benoit³

et al. 1996

J. Clin. Invest.

155

112

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Highly reactive oxygen species rapidly inactivate nitric oxide (NO), an endothelial product which inhibits platelet activation. We studied platelet inhibition by NO in two brothers with a cerebral thrombotic disorder. Both children had hyperreactive platelets, as determined by whole blood platelet aggregometry and flow cytometric analysis of the platelet surface expression of P-selectin. Mixing experiments showed that the patients' platelets behaved normally in control plasma; however, control platelets suspended in patient plasma were not inhibited by NO. As determined by flow cytometry, in the presence of plasma from either patient there was normal inhibition of the thrombin-induced expression of platelet surface P-selectin by prostacyclin, but not NO. Using a scopoletin assay, we measured a 2.7-fold increase in plasma H 2 O 2 generation in one patient and a 3.4-fold increase in the second patient, both compared with control plasma. Glutathione peroxidase (GSH-Px) activity was decreased in the patients' plasmas compared with control plasma. The addition of exogenous GSH-Px led to restoration of platelet inhibition by NO. These data show that, in these patients' plasmas, impaired metabolism of reactive oxygen species reduces the bioavailability of NO and impairs normal platelet inhibitory mechanisms. These findings suggest that attenuated NO-mediated platelet inhibition produced by increased reactive oxygen species or impaired antioxidant defense may cause a thrombotic disorder in humans. ( J. Clin. Invest. 1996. 97:979-987.) Key words: child • cerebral embolism and thrombosis • blood platelet • nitric oxide • glutathione peroxidase

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“…Platelet activation was determined by flow cytometry as platelet H2O2 fluxes linked to stimulation of platelets by collagen according to the method of Del Principe et al (1991). Catalase was used as inhibitor and to simulate the quenching role of red wine phenolic compounds in some of the ex vivo assays.…”

Section: Haemostatic and Inflammatory Parametersmentioning

confidence: 99%

The influence of a Mediterranean Diet with and without Red Wine on the Haemostatic and Inflammatory Parameters of Subjects with the Metabolic Syndrome

Mansvelt

Fourie

Blackhurst

et al. 2016

SAJEV

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This 8 week study examined whether a Mediterranean diet supplemented with red wine, had an acute impact on subjects diagnosed with the metabolic syndrome. Twelve non-smoking subjects with diagnostic criteria of the metabolic syndrome on minimal medication, consumed a Mediterranean-like diet for 4 weeks respectively without and with red wine. The amount of red wine consumed was 250 ml (26 grams of alcohol) per day for male and 180 ml (19 grams) per day for female participants. A nutrigenetic profile for cardiovascular risk factors was performed on each participant. Fasting blood specimens were taken at baseline, after the diet and after the diet with wine interventions for platelet function, procoagulants FVII and FVIII, von Willebrand's factor, fibrinogen, tissue plasminogen activator, plasminogen activator inhibitor-1, highly sensitive C-reactive protein and oxygen radical absorbance capacity (ORAC). After both periods of diet without wine and with wine, ORAC increased significantly compared to baseline levels. Except for platelet H2O2 fluxes and FVII concentration, none of the haemostatic or inflammatory parameters changed significantly after the intervention periods compared with baseline levels. Genetic risk factors for cardiovascular disease were identified in all study participants and the potential genotypic effects relevant to this study were generally in agreement with expected phenotypic response following the dietary intervention. Our conclusions are that the period of intervention was too short for substantial changes in haemostatic or in inflammatory parameters in subjects who already manifest some changes in their cardiovascular system and who showed diverse genetic profiles underlying increased cardiovascular risk.

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

Cited by 63 publications

References 18 publications

Oxidative stress in blood platelets from schizophrenic patients

Oxidative stress in blood platelets from schizophrenic patients

Decreased platelet inhibition by nitric oxide in two brothers with a history of arterial thrombosis.

The influence of a Mediterranean Diet with and without Red Wine on the Haemostatic and Inflammatory Parameters of Subjects with the Metabolic Syndrome

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