Antioxidant effects of serotonin and L-DOPA on oxidative damages of brain synaptosomes.
- Author:
Sang Soo HAM
1
;
Dong Hyun KIM
;
Suk Ha LEE
;
Yun Sang KIM
;
Chung Soo LEE
Author Information
1. Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, 156-756 South Korea.
- Publication Type:Original Article
- Keywords:
Antioxidant action;
Serotonin;
L-DOPA;
Synaptosomes
- MeSH:
Antioxidants*;
Brain*;
Catalase;
Edetic Acid;
Hydroxyl Radical;
Iron;
Levodopa*;
Lipid Peroxidation;
Neurons;
Oxidants;
Serotonin*;
Synaptosomes*;
tert-Butylhydroperoxide;
Xanthine;
Xanthine Oxidase
- From:The Korean Journal of Physiology and Pharmacology
1999;3(2):147-155
- CountryRepublic of Korea
- Language:English
-
Abstract:
Antioxidant effects of serotonin and L-DOPA on neuronal tissues were examined by studying the oxidative damages of brain synaptosomal components. The study further explored the mechanism by which they exert protective actions. Serotonin and L-DOPA (1 muM to 1 mM) significantly inhibited lipid peroxidation of brain tissues by either Fe2+ and ascorbate or t-butyl hydroperoxide in a dose dependent fashion. Protective effect of serotonin on the peroxidative actions of both systems was greater than that of L-DOPA. Protein oxidation of synaptosomes caused by Fe2+ and ascorbate was attenuated by serotonin and L-DOPA. Protein oxidation more sensitively responded to L-DOPA rather than serotonin. Serotonin and L-DOPA (100 muM) decreased effectively the oxidation of synaptosomal sulfhydryl groups caused by Fe2+ and ascorbate. The production of hydroxyl radical caused by either Fe3+, EDTA, H2O2 and ascorbate or xanthine and xanthine oxidase was significantly decreased by serotonin and L-DOPA (1 mM). Equal concentrations of serotonin and L-DOPA restored synaptosomal Ca2+ uptake decreased by Fe2+ and ascorbate, which is responsible for SOD and catalase. Protective effects of serotonin and L-DOPA on brain synaptosomes may be attributed to their removing action on reactive oxidants, hydroxyl radicals and probably iron-oxygen complex, without chelating action on iron.
