2010; 31(4): 489-496
PubMed PMID: 20802448
Analysis of Variance, Animals, Brain:drug effects, Kidney:drug effects, Lipid Peroxidation:drug effects, Lipopolysaccharides:pharmacology, Liver:drug effects, Male, Malondialdehyde:metabolism, Melatonin:pharmacology, Rats, Rats, Wistar, Serotonin:analogs .
OBJECTIVE: Bacterial lipopolysaccharide (LPS) causes lipid peroxidation (LPO). We have found that LPS induces LPO in vitro, in tissue homogenates in a concentration-dependent manner, the concentration of 400 µg/ml demonstrating the most efficient lipid damaging effect . Both melatonin and its precursor, N-acetylserotonin, must possess antioxidant activities, both in vivo or in vitro, however, following some claims, N-acetylserotonin is a more effective extra- and intracellular antioxidant than melatonin. The aim of our study was to compare the effects of melatonin and N-acetylserotonin on the LPS-induced LPO in vitro.
METHODS: Malondialdehyde (MDA) plus 4-hydroxyalkenal (4-HDA) concentrations were measured as the indices of induced membrane peroxidative damage in brain, liver and kidney homogenates. Both melatonin and N-acetylserotonin were used at increasing concentrations, starting from 0.01-5 mM, together with LPS at one concentration level of 400 µg/ml.
RESULTS: In all the examined tissues, LPS stimulated LPO, while both melatonin and N-acetylserotonin decreased LPS-stimulated LPO. Furthermore, the capacity of N-acetylserotonin reducing LPO was higher than that of melatonin.
CONCLUSIONS: The results of the reported study clearly indicate that N-acetylserotonin is a much stronger antioxidant in vitro than melatonin in terms of reducing oxidative damage to lipid membranes. However, it remains still unclear how the features relate to in vivo circumstances....