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 inNeuroscience letters Vol. 405; no. 1; pp. 89 - 93
Main Authors Piñol-Ripoll, G., Fuentes-Broto, L., Millán-Plano, S., Reyes-Gonzáles, M., Mauri, J.A., Martínez-Ballarín, E., Reiter, R.J., García, J.J.
Format Journal Article
LanguageEnglish
Published Shannon Elsevier Ireland Ltd 11.09.2006
Elsevier
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ISSN0304-3940
1872-7972
DOI10.1016/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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ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2006.06.031