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Melatonin protects PLPC liposomes and LDL towards radical‐induced oxidation
Author(s) -
Marchetti Catherine,
SidahmedAdrar Nazha,
Collin Fabrice,
Jore Daniel,
GardèsAlbert Monique,
BonnefontRousselot Dominique
Publication year - 2011
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/j.1600-079x.2011.00889.x
Subject(s) - melatonin , liposome , chemistry , medicine , pharmacology , biochemistry
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 μ m ] 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 μ m , and one in LDL, i.e., 100 μ m . 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.