5 research outputs found
platelet proaggregating activity of A431 human epidermoid carcinoma cell line is ADP release dependent, complement mediated
Efficacia e tollerabilità della doppia terapia antiaggregante piastrinica con Indobufene e Clopidogrel in pazienti con SCA e allergia documentata all’aspirina, sottoposti a PTCA ed impianto di stent
Carnitine inhibits arachidonic acid turnover, platelet function, and oxidative stress
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