Nicotine protects rat brain mitochondria against experimental injuries
Identifieur interne : 000D56 ( PascalFrancis/Checkpoint ); précédent : 000D55; suivant : 000D57Nicotine 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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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><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0028-3908</s0></fA01><fA02 i1="01"><s0>NEPHBW</s0></fA02><fA03 i2="1"><s0>Neuropharmacology</s0></fA03><fA05><s2>44</s2></fA05><fA06><s2>5</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Nicotine protects rat brain mitochondria against experimental injuries</s1></fA08><fA11 i1="01" i2="1"><s1>CORMIER (A.)</s1></fA11><fA11 i1="02" i2="1"><s1>MORIN (C.)</s1></fA11><fA11 i1="03" i2="1"><s1>ZINI (R.)</s1></fA11><fA11 i1="04" i2="1"><s1>TILLEMENT (J.-P.)</s1></fA11><fA11 i1="05" i2="1"><s1>LAGRUE (G.)</s1></fA11><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></fA14><fA14 i1="02"><s1>Centre de Tabacologie, Hôpital Albert Chenevier</s1><s2>94010 Creteil</s2><s3>FRA</s3><sZ>5 aut.</sZ></fA14><fA20><s1>642-652</s1></fA20><fA21><s1>2003</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>10408</s2><s5>354000110911630100</s5></fA43><fA44><s0>0000</s0><s1>© 2003 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.1/4</s0></fA45><fA47 i1="01" i2="1"><s0>03-0487051</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Neuropharmacology</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>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. 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