TY - JOUR
T1 - N-acetylserotonin suppresses hepatic microsomal membrane rigidity associated with lipid peroxidation
AU - García, Joaquín J.
AU - Reiter, Russel J.
AU - Karbownik, Malgorzata
AU - Calvo, Juan R.
AU - Ortiz, Genaro G.
AU - Tan, Dun Xian
AU - Martínez-Ballarín, Enrique
AU - Acua-Castroviejo, Darío
N1 - Funding Information:
This work was supported in part by the Gobierno de Aragón (Grant No. P077/99-BM) and by Amoun Pharmaceutical.
Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 2001/10/5
Y1 - 2001/10/5
N2 - N-acetylserotonin, the immediate precursor of melatonin in the tryptophan metabolic pathway in the pineal gland, has been reported to be an antioxidant. The aim of this work was to test the effect of N-acetylserotonin in stabilizing biological membranes against oxidative stress. Hepatic microsomal membranes from male adult rats were incubated with N-acetylserotonin (0.001-3 mM) before inducing lipid peroxidation using FeCl3, ADP and NADPH. Control experiments were done by incubating microsomal membranes with N-acetylserotonin in the absence of lipid peroxidation-inducing drugs. Membrane fluidity was assessed by fluorescence spectroscopy and malonaldehyde plus 4-hydroxyalkenals concentrations were measured to estimate the degree of lipid peroxidation. 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 of lipid peroxidation, N-acetylserotonin (0.001-3 mM) did not change membrane fluidity nor malonaldehyde plus 4-hydroxyalkenals levels. These results suggest that the protective role of N-acetylserotonin in preserving optimal levels of fluidity of the biological membranes may be related to its ability to reduce lipid peroxidation.
AB - N-acetylserotonin, the immediate precursor of melatonin in the tryptophan metabolic pathway in the pineal gland, has been reported to be an antioxidant. The aim of this work was to test the effect of N-acetylserotonin in stabilizing biological membranes against oxidative stress. Hepatic microsomal membranes from male adult rats were incubated with N-acetylserotonin (0.001-3 mM) before inducing lipid peroxidation using FeCl3, ADP and NADPH. Control experiments were done by incubating microsomal membranes with N-acetylserotonin in the absence of lipid peroxidation-inducing drugs. Membrane fluidity was assessed by fluorescence spectroscopy and malonaldehyde plus 4-hydroxyalkenals concentrations were measured to estimate the degree of lipid peroxidation. 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 of lipid peroxidation, N-acetylserotonin (0.001-3 mM) did not change membrane fluidity nor malonaldehyde plus 4-hydroxyalkenals levels. These results suggest that the protective role of N-acetylserotonin in preserving optimal levels of fluidity of the biological membranes may be related to its ability to reduce lipid peroxidation.
KW - Lipid peroxidation
KW - Membrane fluidity
KW - Microsome
KW - N-acetylserotonin
UR - http://www.scopus.com/inward/record.url?scp=0035812620&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035812620&partnerID=8YFLogxK
U2 - 10.1016/S0014-2999(01)01342-5
DO - 10.1016/S0014-2999(01)01342-5
M3 - Article
C2 - 11675033
AN - SCOPUS:0035812620
VL - 428
SP - 169
EP - 175
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
SN - 0014-2999
IS - 2
ER -