How does fluoroaluminate activate human platelets?

Rendu, Francine; Lebret, Marius; Tenza, Danièle; Lévy-Toledano, S

doi:10.1042/bj2650343

Cited by 16 publications

(11 citation statements)

References 36 publications

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“…These authors proposed that the fluoroaluminate complex, formed upon the association of NaF and AlCl 3 , may be responsible for the observed effects. We have shown here that Al 3+ , at concentrations higher than those used by Rendu et al (11), promoted platelet aggregation and peroxidation in the absence of NaF. Recently, Al 3+ has been shown to induce lipid peroxidation in brain tissue of mice chronically exposed to the metal (6).…”

Section: Discussionmentioning

confidence: 75%

“…Earlier, Rendu et al (11) reported that Al 3+ at concentrations similar to those present in the blood circulation potentiated NaF-elicited platelet aggregation, as well as diacylglycerol and 43-kDa phosphorylation. These authors proposed that the fluoroaluminate complex, formed upon the association of NaF and AlCl 3 , may be responsible for the observed effects.…”

Section: Discussionmentioning

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: 75%

Section: Discussionmentioning

confidence: 99%

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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“…Activation of platelets is connected with shape changes. Rendu et al [78] observed that incubation of platelets with NaF (5-10 mM) induced only slight morphological changes. Addition of 10 M AlCl 3 resulted in aggregation.…”

Section: Plateletsmentioning

confidence: 99%

Fluoride Interactions: From Molecules to Disease

Strunecká¹,

Patočka²,

Blaylock³

et al. 2007

CST

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Fluoride has long been known to influence the activity of various enzymes in vitro. Later it has been demonstrated that many effects primarily attributed to fluoride are caused by synergistic action of fluoride plus aluminum. Aluminofluoride complexes have been widely used as analogues of phosphate groups to study phosphoryl transfer reactions and heterotrimeric G proteins involvement. A number of reports on their use have appeared, with far-reaching consequences for our understanding of fundamental biological processes. Fluoride plus aluminum send false messages, which are amplified by processes of signal transduction. Many investigations of the longterm administration of fluoride to laboratory animals have demonstrated that fluoride and aluminofluoride complexes can elicit impairment of homeostasis, growth, development, cognition, and behavior. Ameliorative effects of calcium, vitamins C, D, and E have been reported. Numerous epidemiological, ecological, and clinical studies have shown the effects of fluoride on humans. Millions of people live in endemic fluorosis areas. A review of fluoride interactions from molecules to disease is necessary for a sound scientific assessment of health risks, which may be linked to the chronic intake of small doses of fluoride and aluminum from environmental and artificial sources.

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“…AIF 4 induces platelet activation by mechanisms not fully elucidated. This compound (10 mM or less) produces diacylglycerol and TxB2, without activating PLC, and increases PKC activity without an apparent increase of intracellular Ca 2+ [15]. At higher concentrations (20 mM or more), A1F 4 activates PLC and liberates TxB2 being the two events independent [7,14].…”

Section: Introductionmentioning

confidence: 99%