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

P. Pignatelli, L. Lenti, V. Sanguigni, G. Frati, I. Simeoni, P. P. Gazzaniga, F. M. Pulcinelli, F. Violi

Research output: Contribution to journalArticlepeer-review


Carnitine is a physiological cellular constituent that favors intracellular fatty acid transport, whose role on platelet function and O2 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 μM) 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 A2 formation, and Ca2+ mobilization, without affecting phospholipase A2 activation. Furthermore, carnitine inhibited platelet superoxide anion (O2 -) 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 O2 - formation, suggesting a role for NADPH oxidase in arachidonic acid-mediated platelet O2 - 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 μM 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.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1 53-1
Publication statusPublished - Jan 1 2003


  • Oxygen free radicals

ASJC Scopus subject areas

  • Physiology


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