Protective effect of melatonin and pinoline on nitric oxide-induced lipid and protein peroxidation in rat brain homogenates

G. Piñol-Ripoll; L. Fuentes-Broto; S. Millán-Plano; M. Reyes-Gonzáles; J. A. Mauri; E. Martínez-Ballarín; R. J. Reiter; J. J. García

doi:10.1016/j.neulet.2006.06.031

Protective effect of melatonin and pinoline on nitric oxide-induced lipid and protein peroxidation in rat brain homogenates

G. Piñol-Ripoll, L. Fuentes-Broto, S. Millán-Plano, M. Reyes-Gonzáles, J. A. Mauri, E. Martínez-Ballarín, R. J. Reiter, J. J. García

Department of Cell Systems & Anatomy

Research output: Contribution to journal › Article › peer-review

18 Scopus citations

Abstract

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 (O₂^-) 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.

Original language	English (US)
Pages (from-to)	89-93
Number of pages	5
Journal	Neuroscience Letters
Volume	405
Issue number	1-2
DOIs	https://doi.org/10.1016/j.neulet.2006.06.031
State	Published - Sep 11 2006

Keywords

Lipid peroxidation
Melatonin
Nitric oxide
Pinoline
Protein peroxidation

ASJC Scopus subject areas

Neuroscience(all)

Access to Document

10.1016/j.neulet.2006.06.031

Cite this

@article{81dde16e25d14048b7e6899b988a5180,

title = "Protective effect of melatonin and pinoline on nitric oxide-induced lipid and protein peroxidation in rat brain homogenates",

abstract = "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 (O2-) 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.",

keywords = "Lipid peroxidation, Melatonin, Nitric oxide, Pinoline, Protein peroxidation",

author = "G. Pi{\~n}ol-Ripoll and L. Fuentes-Broto and S. Mill{\'a}n-Plano and M. Reyes-Gonz{\'a}les and Mauri, {J. A.} and E. Mart{\'i}nez-Ballar{\'i}n and Reiter, {R. J.} and Garc{\'i}a, {J. J.}",

note = "Funding Information: This work was supported in par by the University of Zaragoza (Grant No. IBE2004B-BIO-02), the Gobierno de Arag{\'o}n (Aging and Oxidative Stress Physiology, Grant No. B40) and by FIS from Instituto de Salud Carlos III (Grant No. G03/137).",

year = "2006",

month = sep,

day = "11",

doi = "10.1016/j.neulet.2006.06.031",

language = "English (US)",

volume = "405",

pages = "89--93",

journal = "Neuroscience Letters",

issn = "0304-3940",

publisher = "Elsevier Ireland Ltd",

number = "1-2",

}

TY - JOUR

T1 - Protective effect of melatonin and pinoline on nitric oxide-induced lipid and protein peroxidation in rat brain homogenates

AU - Piñol-Ripoll, G.

AU - Fuentes-Broto, L.

AU - Millán-Plano, S.

AU - Reyes-Gonzáles, M.

AU - Mauri, J. A.

AU - Martínez-Ballarín, E.

AU - Reiter, R. J.

AU - García, J. J.

N1 - Funding Information: This work was supported in par by the University of Zaragoza (Grant No. IBE2004B-BIO-02), the Gobierno de Aragón (Aging and Oxidative Stress Physiology, Grant No. B40) and by FIS from Instituto de Salud Carlos III (Grant No. G03/137).

PY - 2006/9/11

Y1 - 2006/9/11

N2 - 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 (O2-) 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.

AB - 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 (O2-) 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.

KW - Lipid peroxidation

KW - Melatonin

KW - Nitric oxide

KW - Pinoline

KW - Protein peroxidation

UR - http://www.scopus.com/inward/record.url?scp=33746514547&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33746514547&partnerID=8YFLogxK

U2 - 10.1016/j.neulet.2006.06.031

DO - 10.1016/j.neulet.2006.06.031

M3 - Article

C2 - 16854526

AN - SCOPUS:33746514547

SN - 0304-3940

VL - 405

SP - 89

EP - 93

JO - Neuroscience Letters

JF - Neuroscience Letters

IS - 1-2

ER -

Protective effect of melatonin and pinoline on nitric oxide-induced lipid and protein peroxidation in rat brain homogenates

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this