Nicotine protects rat brain mitochondria against experimental injuries
Identifieur interne : 003719 ( Main/Merge ); précédent : 003718; suivant : 003720Nicotine protects rat brain mitochondria against experimental injuries
Auteurs : A. Cormier [France] ; C. Morin [France] ; R. Zini [France] ; J.-P. Tillement [France] ; G. Lagrue [France]Source :
- Neuropharmacology [ 0028-3908 ] ; 2003.
Abstract
Epidemiological studies have reported that cigarette smoking may protect from neurodegenerative diseases such as Parkinson's disease. These protective effects are thought to be mediated by nicotine. Recent data showed that nicotine significantly decreases respiratory control ratio (RCR) and superoxide anion generation of brain mitochondria. Thus, we investigated nicotine effects on rat brain in two experimental models: first, an in vitro anoxia/reoxygenation experiment and secondly, an in vivo rotenone-induced Parkinson-like syndrome. Anoxia/reoxygenation impaired mitochondrial respiration by 43.68% whereas in the presence of nicotine, it was less impaired, by 31.1% at 10-7 M. In rats chronically administered rotenone (3 mg/kg/day), we observed profound mitochondrial damage: the RCR decreased by 50.36% and the superoxide anion generation and the membrane anisotropy increased by 56.03 and 13.43%, respectively. All of these indications of mitochondrial damage were limited by chronic administration of nicotine. Nicotine developed mitochondrial effects in vivo and in vitro at very low concentration. All these results were in accordance with epidemiological studies, which report a protective effect of nicotine in neurodegenerative diseases. Thus, we propose that one effect of nicotine is to preserve mitochondrial functions of the rat central nervous system.
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Cormier</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Laboratoire de Pharmacologie, Department de Pharmacologie, Faculté de Médecine de Paris XII, 8 rue de General Sarrail</s1><s2>94010 Creteil</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Creteil</settlement></placeName></affiliation></author><author><name sortKey="Morin, C" sort="Morin, C" uniqKey="Morin C" first="C." last="Morin">C. Morin</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Laboratoire de Pharmacologie, Department de Pharmacologie, Faculté de Médecine de Paris XII, 8 rue de General Sarrail</s1><s2>94010 Creteil</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Creteil</settlement></placeName></affiliation></author><author><name sortKey="Zini, R" sort="Zini, R" uniqKey="Zini R" first="R." last="Zini">R. Zini</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Laboratoire de Pharmacologie, Department de Pharmacologie, Faculté de Médecine de Paris XII, 8 rue de General Sarrail</s1><s2>94010 Creteil</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Creteil</settlement></placeName></affiliation></author><author><name sortKey="Tillement, J P" sort="Tillement, J P" uniqKey="Tillement J" first="J.-P." last="Tillement">J.-P. Tillement</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Laboratoire de Pharmacologie, Department de Pharmacologie, Faculté de Médecine de Paris XII, 8 rue de General Sarrail</s1><s2>94010 Creteil</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Creteil</settlement></placeName></affiliation></author><author><name sortKey="Lagrue, G" sort="Lagrue, G" uniqKey="Lagrue G" first="G." last="Lagrue">G. Lagrue</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>Centre de Tabacologie, Hôpital Albert Chenevier</s1><s2>94010 Creteil</s2><s3>FRA</s3><sZ>5 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Creteil</settlement></placeName></affiliation></author></analytic><series><title level="j" type="main">Neuropharmacology</title><title level="j" type="abbreviated">Neuropharmacology</title><idno type="ISSN">0028-3908</idno><imprint><date when="2003">2003</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neuropharmacology</title><title level="j" type="abbreviated">Neuropharmacology</title><idno type="ISSN">0028-3908</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Epidemiological studies have reported that cigarette smoking may protect from neurodegenerative diseases such as Parkinson's disease. These protective effects are thought to be mediated by nicotine. Recent data showed that nicotine significantly decreases respiratory control ratio (RCR) and superoxide anion generation of brain mitochondria. Thus, we investigated nicotine effects on rat brain in two experimental models: first, an in vitro anoxia/reoxygenation experiment and secondly, an in vivo rotenone-induced Parkinson-like syndrome. Anoxia/reoxygenation impaired mitochondrial respiration by 43.68% whereas in the presence of nicotine, it was less impaired, by 31.1% at 10<sup>-7</sup> M. In rats chronically administered rotenone (3 mg/kg/day), we observed profound mitochondrial damage: the RCR decreased by 50.36% and the superoxide anion generation and the membrane anisotropy increased by 56.03 and 13.43%, respectively. All of these indications of mitochondrial damage were limited by chronic administration of nicotine. Nicotine developed mitochondrial effects in vivo and in vitro at very low concentration. All these results were in accordance with epidemiological studies, which report a protective effect of nicotine in neurodegenerative diseases. Thus, we propose that one effect of nicotine is to preserve mitochondrial functions of the rat central nervous system.</div></front></TEI><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Creteil</li></settlement></list><tree><country name="France"><region name="Île-de-France"><name sortKey="Cormier, A" sort="Cormier, A" uniqKey="Cormier A" first="A." last="Cormier">A. Cormier</name></region><name sortKey="Lagrue, G" sort="Lagrue, G" uniqKey="Lagrue G" first="G." last="Lagrue">G. Lagrue</name><name sortKey="Morin, C" sort="Morin, C" uniqKey="Morin C" first="C." last="Morin">C. Morin</name><name sortKey="Tillement, J P" sort="Tillement, J P" uniqKey="Tillement J" first="J.-P." last="Tillement">J.-P. Tillement</name><name sortKey="Zini, R" sort="Zini, R" uniqKey="Zini R" first="R." last="Zini">R. Zini</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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