Carnitine is a physiological cellular constituent that favors intracellular fatty acid transport, whose role on platelet function and O-2 free radicals has not been fully investigated. The aim of this study was to seek whether carnitine interferes with arachidonic acid metabolism and platelet function. Carnitine (10-50 muM) was able to dose dependently inhibit arachidonic acid incorporation into platelet phospholipids and agonist-induced arachidonic acid release. Incubation of platelets with carnitine dose dependently inhibited collagen-induced platelet aggregation, thromboxane A(2) formation, and Ca2+ mobilization, without affecting phospholipase A(2) activation. Furthermore, carnitine inhibited platelet superoxide anion (O-2(-)) formation elicited by arachidonic acid and collagen. To explore the underlying mechanism, arachidonic acid-stimulated platelets were incubated with NADPH. This study showed an enhanced platelet O-2(-) formation, suggesting a role for NADPH oxidase in arachidonic acid-mediated platelet O-2(-) production. Incubation of platelets with carnitine significantly reduced arachidonic acid-mediated NADPH oxidase activation. Moreover, the activation of protein kinase C was inhibited by 50 muM carnitine. This study shows that carnitine inhibits arachidonic acid accumulation into platelet phospholipids and in turn platelet function and arachidonic acid release elicited by platelet agonists.

Pignatelli, P., Lenti, L., Sanguigni, V., Frati, G., Simeoni, I., Gazzaniga, P.p., et al. (2003). Carnitine inhibits arachidonic acid turnover, platelet function, and oxidative stress.

Carnitine inhibits arachidonic acid turnover, platelet function, and oxidative stress

SANGUIGNI, VALERIO;
2003-01-01

Abstract

Carnitine is a physiological cellular constituent that favors intracellular fatty acid transport, whose role on platelet function and O-2 free radicals has not been fully investigated. The aim of this study was to seek whether carnitine interferes with arachidonic acid metabolism and platelet function. Carnitine (10-50 muM) was able to dose dependently inhibit arachidonic acid incorporation into platelet phospholipids and agonist-induced arachidonic acid release. Incubation of platelets with carnitine dose dependently inhibited collagen-induced platelet aggregation, thromboxane A(2) formation, and Ca2+ mobilization, without affecting phospholipase A(2) activation. Furthermore, carnitine inhibited platelet superoxide anion (O-2(-)) formation elicited by arachidonic acid and collagen. To explore the underlying mechanism, arachidonic acid-stimulated platelets were incubated with NADPH. This study showed an enhanced platelet O-2(-) formation, suggesting a role for NADPH oxidase in arachidonic acid-mediated platelet O-2(-) production. Incubation of platelets with carnitine significantly reduced arachidonic acid-mediated NADPH oxidase activation. Moreover, the activation of protein kinase C was inhibited by 50 muM carnitine. This study shows that carnitine inhibits arachidonic acid accumulation into platelet phospholipids and in turn platelet function and arachidonic acid release elicited by platelet agonists.
2003
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/09 - MEDICINA INTERNA
English
oxygen free radicals
Pignatelli, P., Lenti, L., Sanguigni, V., Frati, G., Simeoni, I., Gazzaniga, P.p., et al. (2003). Carnitine inhibits arachidonic acid turnover, platelet function, and oxidative stress.
Pignatelli, P; Lenti, L; Sanguigni, V; Frati, G; Simeoni, I; Gazzaniga, Pp; Pulcinelli, Fm; Violi, F
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/50444
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