Dysfunction of mitochondrial complex I and the proteasome: interactions between two biochemical deficits in a cellular model of Parkinson's disease
Identifieur interne : 000577 ( PascalFrancis/Curation ); précédent : 000576; suivant : 000578Dysfunction of mitochondrial complex I and the proteasome: interactions between two biochemical deficits in a cellular model of Parkinson's disease
Auteurs : Günter U. Höglinger [France] ; Géraldine Carrard [France] ; Patrick P. Michel [France] ; Fadia Medja [France] ; Anne Lombes [France] ; Merle Ruberg [France] ; Bertrand Friguet [France] ; Etienne C. Hirsch [France]Source :
- Journal of neurochemistry [ 0022-3042 ] ; 2003.
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Abstract
Two biochemical deficits have been described in the substantia nigra in Parkinson's disease, decreased activity of mitochondrial complex I and reduced proteasomal activity. We analysed interactions between these deficits in primary mesencephalic cultures. Proteasome inhibitors (epoxomicin, MG132) exacerbated the toxicity of complex I inhibitors [rotenone, 1-methyl-4-phenylpyridinium (MPP+)] and of the toxic dopamine analogue 6-hydroxydopamine, but not of inhibitors of mitochondrial complex II-V or excitotoxins [N-methyl-D-aspartate (NMDA), kainate]. Rotenone and MPP+ increased free radicals and reduced proteasomal activity via adenosine triphosphate (ATP) depletion. 6-hydroxydopamine also increased free radicals, but did not affect ATP levels and increased proteasomal activity, presumably in response to oxidative damage. Proteasome inhibition potentiated the toxicity of rotenone, MPP+ and 6-hydroxydopamine at concentrations at which they increased free radical levels > 40% above baseline, exceeding the cellular capacity to detoxify oxidized proteins reduced by proteasome inhibition, and also exacerbated ATP depletion caused by complex I inhibition. Consistently, both free radical scavenging and stimulation of ATP production by glucose supplementation protected against the synergistic toxicity. In summary, proteasome inhibition increases neuronal vulnerability to normally subtoxic levels of free radicals and amplifies energy depletion following complex I inhibition.
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Höglinger</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Carrard, Geraldine" sort="Carrard, Geraldine" uniqKey="Carrard G" first="Géraldine" last="Carrard">Géraldine Carrard</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Laboratoire de Biologie et Biochimie Cellulaire du Vieillissement, Université Paris 7 - Denis Diderot</s1><s2>Paris</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Michel, Patrick P" sort="Michel, Patrick P" uniqKey="Michel P" first="Patrick P." last="Michel">Patrick P. Michel</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Medja, Fadia" sort="Medja, Fadia" uniqKey="Medja F" first="Fadia" last="Medja">Fadia Medja</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>INSERM U582, Institut de Myologie, Hôpital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Lombes, Anne" sort="Lombes, Anne" uniqKey="Lombes A" first="Anne" last="Lombes">Anne Lombes</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>INSERM U582, Institut de Myologie, Hôpital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Ruberg, Merle" sort="Ruberg, Merle" uniqKey="Ruberg M" first="Merle" last="Ruberg">Merle Ruberg</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Friguet, Bertrand" sort="Friguet, Bertrand" uniqKey="Friguet B" first="Bertrand" last="Friguet">Bertrand Friguet</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Laboratoire de Biologie et Biochimie Cellulaire du Vieillissement, Université Paris 7 - Denis Diderot</s1><s2>Paris</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C." last="Hirsch">Etienne C. Hirsch</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>France</country></affiliation></author></analytic><series><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno><imprint><date when="2003">2003</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosine</term><term>Animal</term><term>Cell respiration</term><term>Complex I</term><term>Dopamine</term><term>Dysfunction</term><term>Free radical</term><term>Locus niger</term><term>Mitochondria</term><term>Multicatalytic endopeptidase complex</term><term>Parkinson disease</term><term>Rat</term><term>Toxicity</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Trouble fonctionnel</term><term>Multicatalytic endopeptidase complex</term><term>Locus niger</term><term>Toxicité</term><term>Dopamine</term><term>Respiration cellulaire</term><term>Mitochondrie</term><term>Radical libre</term><term>Parkinson maladie</term><term>Adénosine</term><term>Animal</term><term>Rat</term><term>Complexe I</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Two biochemical deficits have been described in the substantia nigra in Parkinson's disease, decreased activity of mitochondrial complex I and reduced proteasomal activity. We analysed interactions between these deficits in primary mesencephalic cultures. Proteasome inhibitors (epoxomicin, MG132) exacerbated the toxicity of complex I inhibitors [rotenone, 1-methyl-4-phenylpyridinium (MPP<sup>+</sup>)] and of the toxic dopamine analogue 6-hydroxydopamine, but not of inhibitors of mitochondrial complex II-V or excitotoxins [N-methyl-D-aspartate (NMDA), kainate]. Rotenone and MPP<sup>+</sup> increased free radicals and reduced proteasomal activity via adenosine triphosphate (ATP) depletion. 6-hydroxydopamine also increased free radicals, but did not affect ATP levels and increased proteasomal activity, presumably in response to oxidative damage. Proteasome inhibition potentiated the toxicity of rotenone, MPP<sup>+</sup> and 6-hydroxydopamine at concentrations at which they increased free radical levels > 40% above baseline, exceeding the cellular capacity to detoxify oxidized proteins reduced by proteasome inhibition, and also exacerbated ATP depletion caused by complex I inhibition. Consistently, both free radical scavenging and stimulation of ATP production by glucose supplementation protected against the synergistic toxicity. In summary, proteasome inhibition increases neuronal vulnerability to normally subtoxic levels of free radicals and amplifies energy depletion following complex I inhibition.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-3042</s0></fA01><fA02 i1="01"><s0>JONRA9</s0></fA02><fA03 i2="1"><s0>J. neurochem.</s0></fA03><fA05><s2>86</s2></fA05><fA06><s2>5</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Dysfunction of mitochondrial complex I and the proteasome: interactions between two biochemical deficits in a cellular model of Parkinson's disease</s1></fA08><fA11 i1="01" i2="1"><s1>HÖGLINGER (Günter U.)</s1></fA11><fA11 i1="02" i2="1"><s1>CARRARD (Géraldine)</s1></fA11><fA11 i1="03" i2="1"><s1>MICHEL (Patrick P.)</s1></fA11><fA11 i1="04" i2="1"><s1>MEDJA (Fadia)</s1></fA11><fA11 i1="05" i2="1"><s1>LOMBES (Anne)</s1></fA11><fA11 i1="06" i2="1"><s1>RUBERG (Merle)</s1></fA11><fA11 i1="07" i2="1"><s1>FRIGUET (Bertrand)</s1></fA11><fA11 i1="08" i2="1"><s1>HIRSCH (Etienne C.)</s1></fA11><fA14 i1="01"><s1>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></fA14><fA14 i1="02"><s1>Laboratoire de Biologie et Biochimie Cellulaire du Vieillissement, Université Paris 7 - Denis Diderot</s1><s2>Paris</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>7 aut.</sZ></fA14><fA14 i1="03"><s1>INSERM U582, Institut de Myologie, Hôpital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA20><s1>1297-1307</s1></fA20><fA21><s1>2003</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>4037</s2><s5>354000112763500240</s5></fA43><fA44><s0>0000</s0><s1>© 2004 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.1/4</s0></fA45><fA47 i1="01" i2="1"><s0>04-0119254</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of neurochemistry</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Two biochemical deficits have been described in the substantia nigra in Parkinson's disease, decreased activity of mitochondrial complex I and reduced proteasomal activity. We analysed interactions between these deficits in primary mesencephalic cultures. Proteasome inhibitors (epoxomicin, MG132) exacerbated the toxicity of complex I inhibitors [rotenone, 1-methyl-4-phenylpyridinium (MPP<sup>+</sup>)] and of the toxic dopamine analogue 6-hydroxydopamine, but not of inhibitors of mitochondrial complex II-V or excitotoxins [N-methyl-D-aspartate (NMDA), kainate]. Rotenone and MPP<sup>+</sup> increased free radicals and reduced proteasomal activity via adenosine triphosphate (ATP) depletion. 6-hydroxydopamine also increased free radicals, but did not affect ATP levels and increased proteasomal activity, presumably in response to oxidative damage. Proteasome inhibition potentiated the toxicity of rotenone, MPP<sup>+</sup> and 6-hydroxydopamine at concentrations at which they increased free radical levels > 40% above baseline, exceeding the cellular capacity to detoxify oxidized proteins reduced by proteasome inhibition, and also exacerbated ATP depletion caused by complex I inhibition. Consistently, both free radical scavenging and stimulation of ATP production by glucose supplementation protected against the synergistic toxicity. 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syndrome</s0><s5>21</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>21</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>21</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>22</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>22</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>22</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>23</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>23</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>23</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>24</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>24</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>24</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>25</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Central nervous system</s0><s5>25</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>25</s5></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Neurotransmetteur</s0><s5>32</s5></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Neurotransmitter</s0><s5>32</s5></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Neurotransmisor</s0><s5>32</s5></fC07><fC07 i1="11" i2="X" l="FRE"><s0>Catécholamine</s0><s5>33</s5></fC07><fC07 i1="11" i2="X" l="ENG"><s0>Catecholamine</s0><s5>33</s5></fC07><fC07 i1="11" i2="X" l="SPA"><s0>Catecolamina</s0><s5>33</s5></fC07><fC07 i1="12" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="14" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="14" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="14" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fN21><s1>075</s1></fN21></pA></standard></inist></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Dysfunction of mitochondrial complex I and the proteasome: interactions between two biochemical deficits in a cellular model of Parkinson's disease
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