N-acetylserotonin suppresses hepatic microsomal membrane rigidity associated with lipid

N-acetylserotonin, the immediate precursor of melatonin in the tryptophan m etabolic pathway in the pineal gland, has been reported to be an antioxidan t. The aim of this work was to test the effect of N-acetylserotonin in stab ilizing biological membranes against oxidative stress. Hepatic microsomal m embranes from male adult rats were incubated with N-acetylserotonin (0.001- 3 mM) before inducing lipid peroxidation using FeCl3, ADP and NADPH, Contro l experiments were done by incubating microsomal membranes with N-acetylser otonin in the absence of lipid peroxidation-inducing drugs. Membrane fluidi ty was assessed by fluorescence spectroscopy and malonaldehyde plus 4-hydro xyalkenals concentrations were measured to estimate the degree of lipid per oxidation. Free radicals induced by the combination of FeCl3 + ADP + NADPH produced a significant decrease in the microsomal membrane fluidity, which was associated with an increase in the malonaldehyde plus 4-hydroxyalkenals levels. These changes were suppressed in a concentration-dependent manner when N-acetylserotonin was added in the incubation buffer. In the absence o f lipid peroxidation, N-acetylserotonin (0.001-3 mM) did not change membran e fluidity nor malonaldehyde plus 4-hydroxyalkenals levels. These results s uggest that the protective role of N-acetylserotonin in preserving optimal levels of fluidity of the biological membranes may be related to its abilit y to reduce lipid peroxidation. (C) 2001 Elsevier Science B.V. All rights r eserved.