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Melatonin protects PLPC liposomes and LDL towards radical-induced oxidation


Address reprint requests to Dominique Bonnefont-Rousselot, Département de Biologie Expérimentale, Métabolique et Clinique, EA 4466, Faculté des Sciences Pharmaceutiques et Biologiques, Université Paris Descartes, 4, avenue de l’Observatoire, 75006 Paris, France.


Abstract:  This study investigated the in vitro protective effects of melatonin against oxidation of 1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphocholine (PLPC) liposomes [(PLPC) = 250 μm] and low-density lipoproteins (LDL, 3 g/L total concentration) by hydroxyl radicals produced by water gamma radiolysis. Conjugated dienes (CD) and hydroperoxides from cholesteryl esters (CEOOH) and phospholipids (PCOOH) were measured as indices of lipid peroxidation. Protein (apoB) oxidation in LDL was assessed by carbonyl groups. Two LDL antioxidants (vitamin E and β-carotene) were monitored as a function of the radiation dose. Three concentrations of melatonin were studied in PLPC liposomes, i.e., 20, 50 and 100 μm, and one in LDL, i.e., 100 μm. Melatonin consumption was also followed up in both lipid models upon irradiation, together with the residual PLPC concentration in liposomes. In PLPC liposomes, scavenging of lipid-derived peroxyl radicals was not the only phenomenon to explain the protective properties of melatonin towards lipid peroxidation. Indeed, melatonin also reacted with hydroxyl radicals generated in aqueous phase, which led us to suggest that hydroxyl radicals reacted relatively slowly with PLPC. Melatonin was efficient in lowering lipid peroxidation in LDL, as shown by the decrease in the formation of CDs and in hydroperoxides. Moreover, melatonin clearly slowed radio-induced apolipoprotein B carbonylation and protected α-tocopherol and β-carotene in LDL.