We here report the activity of the neurohormone melatonin (MLT) as a s
cavenger of free radicals in two different experimental models: (a) li
noleic acid peroxidation initiated by different free radical-generatin
g systems and (b) a multilamellar vesicle system composed of dilinoleo
ylphosphatidylcholine. In system (a) linoleic acid peroxidation, induc
ed by either the water-soluble initiator 2,2'-azobis (2-amidinopropane
) dihydrochloride(ABAP) or Fe2+-EDTA addition to 2.6 mM linoleic acid
dispersed in SDS-phosphate buffer, was evaluated as the formation of c
onjugated dienes, measured spectrophotometrically at 236 nm. MLT did n
ot reduce the rate of peroxidation induced by ABAP, but did reduce, in
a concentration-dependent fashion, the rate of the reaction activated
by Fe2+-EDTA. In system (b) multilamellar vesicles were used as the s
ubstrate for lipid peroxidation, initiated by Fe2+-EDTA and determined
by means of malonaldehyde (MDA) and 4-hydroxyalkenal (4-HDA) content.
MLT was found to be slightly more effective in system (b) than in the
dispersed linoleic acid system (see a). These results show that MLT i
nhibits lipid damage induced by oxygen free radicals. However, MLT is
only about one one-hundredth as effective an antioxidant as vitamin E
in the micelles system.