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Am J Physiol Heart Circ Physiol 284: H41-H48, 2003. First published September 5, 2002; doi:10.1152/ajpheart.00249.2002
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Vol. 284, Issue 1, H41-H48, January 2003

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

P. Pignatelli1, L. Lenti1, V. Sanguigni3, G. Frati2, I. Simeoni1, P. P. Gazzaniga1, F. M. Pulcinelli1, and F. Violi1

1 Dipartimento di Medicina Sperimentale e Patologia, Università di Roma La Sapienza, 00185 Rome; 2 Istituto di Chirurgia Toracica e Cardiovascolare, Università di Siena, 0577 Siena; and 3 Dipartimento di Medicina Interna, Università di Roma Tor Vergata, 00100 Rome, Italy

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 (O<UP><SUB>2</SUB><SUP>−</SUP></UP>) 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<UP><SUB>2</SUB><SUP>−</SUP></UP> formation, suggesting a role for NADPH oxidase in arachidonic acid-mediated platelet O<UP><SUB>2</SUB><SUP>−</SUP></UP> 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.

oxygen free radicals


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