Titre
Vitamin C blocks inflammatory platelet-activating factor mimetics created by cigarette smoking.
Type
article
Institution
Externe
Périodique
Auteur(s)
Lehr, H.A.
Auteure/Auteur
Weyrich, A.S.
Auteure/Auteur
Saetzler, R.K.
Auteure/Auteur
Jurek, A.
Auteure/Auteur
Arfors, K.E.
Auteure/Auteur
Zimmerman, G.A.
Auteure/Auteur
Prescott, S.M.
Auteure/Auteur
McIntyre, T.M.
Auteure/Auteur
Liens vers les personnes
ISSN
0021-9738
Statut éditorial
Publié
Date de publication
1997
Volume
99
Numéro
10
Première page
2358
Dernière page/numéro d’article
2364
Langue
anglais
Résumé
Cigarette smoking within minutes induces leukocyte adhesion to the vascular wall and formation of intravascular leukocyte-platelet aggregates. We find this is inhibited by platelet-activating factor (PAF) receptor antagonists, and correlates with the accumulation of PAF-like mediators in the blood of cigarette smoke-exposed hamsters. These mediators were PAF-like lipids, formed by nonenzymatic oxidative modification of existing phospholipids, that were distinct from biosynthetic PAF. These PAF-like lipids induced isolated human monocytes and platelets to aggregate, which greatly increased their secretion of IL-8 and macrophage inflammatory protein-1alpha. Both events were blocked by a PAF receptor antagonist. Similarly, blocking the PAF receptor in vivo blocked smoke-induced leukocyte aggregation and pavementing along the vascular wall. Dietary supplementation with the antioxidant vitamin C prevented the accumulation of PAF-like lipids, and it prevented cigarette smoke-induced leukocyte adhesion to the vascular wall and formation of leukocyte-platelet aggregates. This is the first in vivo demonstration of inflammatory phospholipid oxidation products and it suggests a molecular mechanism coupling cigarette smoke with rapid inflammatory changes. Inhibition of PAF-like lipid formation and their intravascular sequela by vitamin C suggests a simple dietary means to reduce smoking-related cardiovascular disease.
Sujets
PID Serval
serval:BIB_F9529143F32B
PMID
Open Access
Oui
Date de création
2011-11-25T18:32:49.522Z
Date de création dans IRIS
2025-05-21T06:54:53Z