Protective effect of melatonin and pinoline on nitric oxide-induced lipid and protein peroxidation in rat brain homogenates
Nitric oxide (NO) is a physiological neurotransmitter, a mediator of the excitatory neurotransmitter glutamate pathways that regulates several neuroendocrine functions, but excessive NO is toxic by itself and it interacts with superoxide radical (O 2 −) to form the peroxynitrite anion (ONOO −). Usin...
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Published in | Neuroscience letters Vol. 405; no. 1; pp. 89 - 93 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Shannon
Elsevier Ireland Ltd
11.09.2006
Elsevier |
Subjects | |
Online Access | Get full text |
ISSN | 0304-3940 1872-7972 |
DOI | 10.1016/j.neulet.2006.06.031 |
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Summary: | Nitric oxide (NO) is a physiological neurotransmitter, a mediator of the excitatory neurotransmitter glutamate pathways that regulates several neuroendocrine functions, but excessive NO is toxic by itself and it interacts with superoxide radical (O
2
−) to form the peroxynitrite anion (ONOO
−). Using rat brain homogenates, we investigated the effects of melatonin and pinoline in preventing the level of lipid peroxidation (LPO) and carbonyl contents in proteins induced by nitric oxide (NO) which was released by the addition of sodium nitroprusside (SNP). Lipid and protein peroxidation were estimated by quantifying malondialdehyde (MDA) and 4-hydroxyalkenal (4-HDA) concentrations and carbonyl contents, respectively. SNP increased MDA
+
4-HDA and carbonyl contents production in brain homogenates in a time and concentration dependent manner. Both, melatonin and pinoline reduced NO-induced LPO and carbonyl contents in a dose-dependent manner in concentrations from 0.03 to 3
mM and 1 to 300
μM, respectively. Under the in vitro conditions of this experiment, both antioxidants were more efficient in limiting SNP protein oxidation than lipid damage. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0304-3940 1872-7972 |
DOI: | 10.1016/j.neulet.2006.06.031 |