Melatonin and structural analogues do not possess antioxidant properties on Fe(2+)-initiated peroxidation of sonicated liposomes made of retinal lipids

Melatonin and its structural analogues display antioxidant activity in vivo but their activity in model membranes is not very well known. In this study, we have investigated the antioxidant capacity of melatonin and structural analogues on Fe(2+)-initiated peroxidation of sonicated liposomes made of retinal lipids. The indoleamines were evaluated against butylated hydroxitoluene (BHT) which was chosen as a reference standard because of its high antioxidant capacity. After the addition of Fe(2+) as initiator of lipid peroxidation, quick production of conjugated dienes was observed. With addition of increasing concentrations of BHT the start of the reaction was delayed and initial reaction rates were lower. However, this reduction was not proportional to the increase in concentration. The start of the reaction and initial reaction rates were not modified in the presence of melatonin and its structural analogues. The formation of TBARS started immediately after the addition of Fe(2+). The increase in the concentration of BHT avoided the emergence of TBARS. Changes were not observed in the presence of melatonin or structural analogues. Retinal lipids showed a high content of docosahexaenoic (22: 6 (Δ4,7,10,13,16,19) acid, characteristic of this tissue. A little bit of that fatty acid was lost when sonicated liposomes were prepared with these retinal lipids. The polyunsaturated fatty acids (PUFAs) diminished significantly after incubation of liposomes with Fe(2+) during 1h. BHT preserved PUFAs whereas melatonin and its related indoleamines did not. These data reinforce the hypothesis that melatonin and structural analogues do not possess antioxidant properties per se in this liposomal model system.