Arachidonic Acid-Induced Chemiluminescence of Human Platelets: Contribution of the Prostaglandin and Lipoxygenase Pathways

Wörner, P.

doi:10.1055/s-0038-1653423

Cited by 19 publications

(6 citation statements)

References 36 publications

(22 reference statements)

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“…There is experimental evidence that lipid peroxides increase platelet sensitivity to agonists (26,27). Furthermore, early reports indicated that CL in platelets arises from prostaglan- din synthesis and lipoxygenase activity (15,16). Worner (15) reported that the chemiluminescence response of platelets exposed to arachidonic acid is dependent on the prostaglandin and lipoxygenase pathways.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, early reports indicated that CL in platelets arises from prostaglan- din synthesis and lipoxygenase activity (15,16). Worner (15) reported that the chemiluminescence response of platelets exposed to arachidonic acid is dependent on the prostaglandin and lipoxygenase pathways. Accordingly, the inhibition of platelet CL measured here in the presence of antioxidants indicates metabolization of arachidonic acid under our experimental conditions.…”

Section: Discussionmentioning

confidence: 99%

“…The enhancement of phospholipase A 2 and phospholipase C activities promotes the mobilization of arachidonic acid from platelet membrane phospholipids resulting in increased synthesis of eicosanoids (13,14). In addition, the generation of oxygen metabolites during prostaglandin synthesis and the lipoxygenase-dependent arachidonic acid turnover is accompanied by light emission from platelets in the presence of luminol (15,16). Luminol-dependent chemiluminescence (CL) is generated through its peroxidase-catalyzed oxidation, and has been used to estimate the oxidative stress status in a number of systems (17).…”

Section: Introductionmentioning

confidence: 99%

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Aluminum induces lipid peroxidation and aggregation of human blood platelets

Neiva¹,

Fries²,

Monteiro³

et al. 1997

Braz J Med Biol Res

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Aluminum (Al 3+ ) intoxication is thought to play a major role in the development of Alzheimer's disease and in certain pathologic manifestations arising from long-term hemodialysis. Although the metal does not present redox capacity, it can stimulate tissue lipid peroxidation in animal models. Furthermore, in vitro studies have revealed that the fluoroaluminate complex induces diacylglycerol formation, 43-kDa protein phosphorylation and aggregation. Based on these observations, we postulated that Al 3+ -induced blood platelet aggregation was mediated by lipid peroxidation. Using chemiluminescence (CL) of luminol as an index of total lipid peroxidation capacity, we established a correlation between lipid peroxidation capacity and platelet aggregation. Al 3+ (20-100 µM) stimulated CL production by human blood platelets as well as their aggregation. Incubation of the platelets with the antioxidants nor-dihydroguaiaretic acid (NDGA) (100 µM) and n-propyl gallate (NPG) (100 µM), inhibitors of the lipoxygenase pathway, completely prevented CL and platelet aggregation. Acetyl salicylic acid (ASA) (100 µM), an inhibitor of the cyclooxygenase pathway, was a weaker inhibitor of both events. These findings suggest that Al 3+ stimulates lipid peroxidation and the lipoxygenase pathway in human blood platelets thereby causing their aggregation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Aluminum induces lipid peroxidation and aggregation of human blood platelets

Neiva¹,

Fries²,

Monteiro³

et al. 1997

Braz J Med Biol Res

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“…Wrrner (39) and Larsen et al (26) showed by use of chemiluminescence that thrombin-stimulated platelets mainly generate OHwhich may injure the endothelial cells. This, indicates that plateletinduced damage to endothelial cells by OH" is not the cause of increased adhesion.…”

Section: Discussionmentioning

confidence: 99%

Addition of both platelets and thrombin in combination accelerates tumor cells to adhere to endothelial cells In vitro

Helland

Klementsen

Jørgensen

1997

In Vitro Cell.Dev.Biol.-Animal

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Platelets and coagulation are involved in the pathogenesis of blood-borne metastases. The aim of this study is to obtain more information about the mechanisms involved in the initial adhesion of tumor cells to endothelial cells. In short term experiments with tumor cells, suspended in the medium of cultured endothelial cells, we tested whether addition of both platelets and thrombin cause more tumor cell adhesion to endothelial cells, than when either platelets or thrombin are acting alone. HeLa cells or HT29 cells, prelabeled with radioactive 51Cr, human platelets, and thrombin were added to human endothelial cell cultures. Following 15 min of shaking at 37 degrees C, the percentage of tumor cell adhesion was calculated. The percentages of adhering tumor cells with the presence of both platelets and thrombin were greatly increased compared to controls. Addition of hirudin 2 min before thrombin lowered the adhesion percentage of tumor cells. Hirudin added immediately before and 2 min after thrombin gave only minor effects. When the endothelium was treated with superoxide dismutase, catalase, and mannitol, the adhesion of tumor cells was lowered with catalase and superoxide dismutase. The cause of tumor cell-endothelial cell interaction is probably complex. Our results show that activated platelets enhance the tumor cell adhesion, and that generation of active oxygen species may be important in the initial phase of the interaction.

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“…The clear effect of arachidonic acid on CL suggests that eicosanoid formation was not affected by washing the cells with PCEp This is an important point since the critical role played by platelet prostaglandin syn thesis and CL was clearly demonstrated [11]. There is also a negligible contribution of the lipoxygenase pathway if arachidonic acid is of endogenous origin [12], which is not the case when exogenous arachidonic acid is added to pla telets thereby avoiding the time course of arachidonic acid turnover via two signals of CL [13]. Our data, which are in opposition to the reports of Ameisen et al [6] and Pearson and Suarez-Mendez [7], could be due to technical differ ences (such as the use of apyrase or the PGE, concentra tion).…”

mentioning

confidence: 95%

In vitro Study of Platelets and Circulating Mononuclear Cells of Subjects Presenting an Intolerance to Aspirin

Guez

Gualde²,

Bezian³

et al. 1992

Int Arch Allergy Immunol

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Aspirine-sensitive asthma (ASA) is a disease defined only by clinical criteria. It is an intrinsic asthma related to a hypersensitivity to aspirin. The illness is linked to abnormalities in platelet and macrophage arachidonic acid metabolism. We assessed in vitro the platelet chemoluminescence (CL) and lymphocyte proliferative response of ASA patients. We observed that platelets from patients and controls do not generate any CL in the presence of aspirin. Concerning the proliferative response of lymphocytes, the in vitro effect of aspirin depends upon the origin of the lymphocytes tested. Thus aspirin clearly enhances the proliferative response of lymphocytes from normal subjects but diminishes the thymidine uptake by lymphocytes from ASA patients. This discrepancy in the in vitro response of lymphocytes from normal subjects and patients might be useful for in vitro diagnosis of ASA.

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Arachidonic Acid-Induced Chemiluminescence of Human Platelets: Contribution of the Prostaglandin and Lipoxygenase Pathways

Cited by 19 publications

References 36 publications

Aluminum induces lipid peroxidation and aggregation of human blood platelets

Aluminum induces lipid peroxidation and aggregation of human blood platelets

Addition of both platelets and thrombin in combination accelerates tumor cells to adhere to endothelial cells In vitro

In vitro Study of Platelets and Circulating Mononuclear Cells of Subjects Presenting an Intolerance to Aspirin

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