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.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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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<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>
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</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Animal</s0>
<s5>14</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Rat</s0>
<s5>54</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Rat</s0>
<s5>54</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Rata</s0>
<s5>54</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Complexe I</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Complex I</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>20</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>20</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>20</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Extrapyramidal 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>
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