Vitamin E consumption induced by oxidative stress in red blood cells is enhanced by melatonin and reduced by N-acetylserotonin.

The effect of melatonin and its precursor N-acetylserotonin was studied in a model of lipid peroxidation induced in human red blood cells by incubation with cumene hydroperoxide (CHP) and H2O2. The oxidative stress was expressed as vitamin E consumption in the presence of melatonin or N-acetylserotonin (concentration ranging from 0.3 to 400 microM): incubation with melatonin not only lacked any protective effect but it induced a dose-dependent extra vitamin E consumption with both CHP and H2O2. On the contrary, N-acetylserotonin showed a strong antioxidant effect at concentrations between 100 and 400 microM. The hydrogen-donating capacity of melatonin and N-acetylserotonin was also evaluated from the decay of the ESR signal of galvinoxyl radical used as hydrogen abstractor. Lack of hydrogen-donating capacity was observed with melatonin, whereas N-acetylserotonin showed a significant hydrogendonating capacity although inferior to vitamin E, thus suggesting that N-acetylserotonin acts by the classical antioxidant mechanism of hydrogen donation. The measurement of the oxidation potential and the specific molecular structure suggest that the vitamin E consumption effect observed with melatonin could be due to the interactions of its radical cation or derivatives on vitamin E.