Mitochondrial respiratory failure in skeletal muscle from patients with Parkinson's disease and multiple system atrophy
Identifieur interne : 001854 ( Istex/Corpus ); précédent : 001853; suivant : 001855Mitochondrial respiratory failure in skeletal muscle from patients with Parkinson's disease and multiple system atrophy
Auteurs : O. Blin ; C. Desnuelle ; O. Rascol ; M. Borg ; H. Peyro Saint Paul ; J. P. Azulay ; F. Billé ; D. Figarella ; F. Coulom ; J. F. Pellissier ; J. L. Montastruc ; M. Chatel ; G. SerratriceSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1994.
Abstract
We studied mitochondrial respiratory chain function in skeletal muscle taken from 27 patients with idiopathic Parkinson's disease (PD; 21 Dopa-treated PD patients and 6 de novo patients), 5 patients with multiple system atrophy (MSA) and from 43 age-matched controls in order to determine the occurrence of mitochondrial respiratory chain abnormalities in parkinsonian syndromes. In our control subjects, we found a significant age-related decrease in the activity of respiratory chain complex I. As compared to carefully age-matched control subjects, activity of complex (NADH: ubiquinone reductase) was significantly lower in muscle mitochondria from patients with PD and MSA and a mean remaining activity < 30% of controls was observed. Mean activities of complexes III (ubiquinol:cytochrome c reductase) and IV (cytochrome c oxidase) were also lower in PD patients than controls, but a low activity (remaining activity < 30% of controls) was observed in only 5 PD patients for complex I and III or I and IV. No deficit in complex II activity (succinate: ubiquinone reductase) was observed. Our results support the hypothesis of a wide-spread mitochondrial complex I deficiency in PD and MSA as compared to age-matched controls, who showed age-related deficiency. This deficit can be found in de novo PD patients as well as in treated patients. The observed respiratory enzyme chain deficiency could not be explained by the dose and duration of l-Dopa or dopaminergic agonist treatment, the severity of the disease, anxiety or depression since no significant correlation was found between these parameters and enzyme complexes activities.
Url:
DOI: 10.1016/0022-510X(94)90248-8
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<front><div type="abstract" xml:lang="en">We studied mitochondrial respiratory chain function in skeletal muscle taken from 27 patients with idiopathic Parkinson's disease (PD; 21 Dopa-treated PD patients and 6 de novo patients), 5 patients with multiple system atrophy (MSA) and from 43 age-matched controls in order to determine the occurrence of mitochondrial respiratory chain abnormalities in parkinsonian syndromes. In our control subjects, we found a significant age-related decrease in the activity of respiratory chain complex I. As compared to carefully age-matched control subjects, activity of complex (NADH: ubiquinone reductase) was significantly lower in muscle mitochondria from patients with PD and MSA and a mean remaining activity < 30% of controls was observed. Mean activities of complexes III (ubiquinol:cytochrome c reductase) and IV (cytochrome c oxidase) were also lower in PD patients than controls, but a low activity (remaining activity < 30% of controls) was observed in only 5 PD patients for complex I and III or I and IV. No deficit in complex II activity (succinate: ubiquinone reductase) was observed. Our results support the hypothesis of a wide-spread mitochondrial complex I deficiency in PD and MSA as compared to age-matched controls, who showed age-related deficiency. This deficit can be found in de novo PD patients as well as in treated patients. The observed respiratory enzyme chain deficiency could not be explained by the dose and duration of l-Dopa or dopaminergic agonist treatment, the severity of the disease, anxiety or depression since no significant correlation was found between these parameters and enzyme complexes activities.</div>
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<abstract>We studied mitochondrial respiratory chain function in skeletal muscle taken from 27 patients with idiopathic Parkinson's disease (PD; 21 Dopa-treated PD patients and 6 de novo patients), 5 patients with multiple system atrophy (MSA) and from 43 age-matched controls in order to determine the occurrence of mitochondrial respiratory chain abnormalities in parkinsonian syndromes. In our control subjects, we found a significant age-related decrease in the activity of respiratory chain complex I. As compared to carefully age-matched control subjects, activity of complex (NADH: ubiquinone reductase) was significantly lower in muscle mitochondria from patients with PD and MSA and a mean remaining activity > 30% of controls was observed. Mean activities of complexes III (ubiquinol:cytochrome c reductase) and IV (cytochrome c oxidase) were also lower in PD patients than controls, but a low activity (remaining activity > 30% of controls) was observed in only 5 PD patients for complex I and III or I and IV. No deficit in complex II activity (succinate: ubiquinone reductase) was observed. Our results support the hypothesis of a wide-spread mitochondrial complex I deficiency in PD and MSA as compared to age-matched controls, who showed age-related deficiency. This deficit can be found in de novo PD patients as well as in treated patients. The observed respiratory enzyme chain deficiency could not be explained by the dose and duration of l-Dopa or dopaminergic agonist treatment, the severity of the disease, anxiety or depression since no significant correlation was found between these parameters and enzyme complexes activities.</abstract>
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<surname>Serratrice</surname>
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<monogr><title level="j">Journal of the Neurological Sciences</title>
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<abstract xml:lang="en"><p>We studied mitochondrial respiratory chain function in skeletal muscle taken from 27 patients with idiopathic Parkinson's disease (PD; 21 Dopa-treated PD patients and 6 de novo patients), 5 patients with multiple system atrophy (MSA) and from 43 age-matched controls in order to determine the occurrence of mitochondrial respiratory chain abnormalities in parkinsonian syndromes. In our control subjects, we found a significant age-related decrease in the activity of respiratory chain complex I. As compared to carefully age-matched control subjects, activity of complex (NADH: ubiquinone reductase) was significantly lower in muscle mitochondria from patients with PD and MSA and a mean remaining activity < 30% of controls was observed. Mean activities of complexes III (ubiquinol:cytochrome c reductase) and IV (cytochrome c oxidase) were also lower in PD patients than controls, but a low activity (remaining activity < 30% of controls) was observed in only 5 PD patients for complex I and III or I and IV. No deficit in complex II activity (succinate: ubiquinone reductase) was observed. Our results support the hypothesis of a wide-spread mitochondrial complex I deficiency in PD and MSA as compared to age-matched controls, who showed age-related deficiency. This deficit can be found in de novo PD patients as well as in treated patients. The observed respiratory enzyme chain deficiency could not be explained by the dose and duration of l-Dopa or dopaminergic agonist treatment, the severity of the disease, anxiety or depression since no significant correlation was found between these parameters and enzyme complexes activities.</p>
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<head><ce:dochead><ce:textfn>Research article</ce:textfn>
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<ce:title>Mitochondrial respiratory failure in skeletal muscle from patients with Parkinson's disease and multiple system atrophy</ce:title>
<ce:author-group><ce:author><ce:given-name>O.</ce:given-name>
<ce:surname>Blin</ce:surname>
<ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup>
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<ce:author><ce:given-name>C.</ce:given-name>
<ce:surname>Desnuelle</ce:surname>
<ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup>
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<ce:author><ce:given-name>O.</ce:given-name>
<ce:surname>Rascol</ce:surname>
<ce:cross-ref refid="AFF5"><ce:sup>e</ce:sup>
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<ce:author><ce:given-name>M.</ce:given-name>
<ce:surname>Borg</ce:surname>
<ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>H.Peyro Saint</ce:given-name>
<ce:surname>Paul</ce:surname>
<ce:cross-ref refid="AFF5"><ce:sup>e</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>J.P.</ce:given-name>
<ce:surname>Azulay</ce:surname>
<ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup>
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</ce:author>
<ce:author><ce:given-name>F.</ce:given-name>
<ce:surname>Billé</ce:surname>
<ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup>
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<ce:author><ce:given-name>D.</ce:given-name>
<ce:surname>Figarella</ce:surname>
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<ce:surname>Coulom</ce:surname>
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<ce:affiliation id="AFF1"><ce:label>a</ce:label>
<ce:textfn>Pharmacologie Médicale et Clinique and CPCET, CHU Timone, 13385 Marseille Cedex 5, France</ce:textfn>
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<ce:affiliation id="AFF2"><ce:label>b</ce:label>
<ce:textfn>Clinique des Maladies du Système nerveux et de l'Appareil Locomoteur, CHU Timone, 13385 Marseille Cedex 5, France</ce:textfn>
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<ce:affiliation id="AFF3"><ce:label>c</ce:label>
<ce:textfn>Département de Neuropathologie, CHU Timone, 13385 Marseille Cedex 5, France</ce:textfn>
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<ce:affiliation id="AFF4"><ce:label>d</ce:label>
<ce:textfn>Service de Neurologie, CHU Pasteur, 06000 Nice, France</ce:textfn>
</ce:affiliation>
<ce:affiliation id="AFF5"><ce:label>e</ce:label>
<ce:textfn>Laboratoire de Pharmacologie Médicale et Clinique, Faculté de Médecine, 31073 Toulouse, France</ce:textfn>
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<ce:text>Corresponding author.</ce:text>
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<ce:date-received day="31" month="8" year="1993"></ce:date-received>
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<ce:abstract><ce:section-title>Abstract</ce:section-title>
<ce:abstract-sec><ce:simple-para>We studied mitochondrial respiratory chain function in skeletal muscle taken from 27 patients with idiopathic Parkinson's disease (PD; 21 Dopa-treated PD patients and 6 de novo patients), 5 patients with multiple system atrophy (MSA) and from 43 age-matched controls in order to determine the occurrence of mitochondrial respiratory chain abnormalities in parkinsonian syndromes. In our control subjects, we found a significant age-related decrease in the activity of respiratory chain complex I. As compared to carefully age-matched control subjects, activity of complex (NADH: ubiquinone reductase) was significantly lower in muscle mitochondria from patients with PD and MSA and a mean remaining activity < 30% of controls was observed. Mean activities of complexes III (ubiquinol:cytochrome <ce:italic>c</ce:italic>
reductase) and IV (cytochrome <ce:italic>c</ce:italic>
oxidase) were also lower in PD patients than controls, but a low activity (remaining activity < 30% of controls) was observed in only 5 PD patients for complex I and III or I and IV. No deficit in complex II activity (succinate: ubiquinone reductase) was observed. Our results support the hypothesis of a wide-spread mitochondrial complex I deficiency in PD and MSA as compared to age-matched controls, who showed age-related deficiency. This deficit can be found in de novo PD patients as well as in treated patients. The observed respiratory enzyme chain deficiency could not be explained by the dose and duration of <ce:small-caps>l</ce:small-caps>
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<ce:keyword><ce:text>Parkinson's disease</ce:text>
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<abstract lang="en">We studied mitochondrial respiratory chain function in skeletal muscle taken from 27 patients with idiopathic Parkinson's disease (PD; 21 Dopa-treated PD patients and 6 de novo patients), 5 patients with multiple system atrophy (MSA) and from 43 age-matched controls in order to determine the occurrence of mitochondrial respiratory chain abnormalities in parkinsonian syndromes. In our control subjects, we found a significant age-related decrease in the activity of respiratory chain complex I. As compared to carefully age-matched control subjects, activity of complex (NADH: ubiquinone reductase) was significantly lower in muscle mitochondria from patients with PD and MSA and a mean remaining activity < 30% of controls was observed. Mean activities of complexes III (ubiquinol:cytochrome c reductase) and IV (cytochrome c oxidase) were also lower in PD patients than controls, but a low activity (remaining activity < 30% of controls) was observed in only 5 PD patients for complex I and III or I and IV. No deficit in complex II activity (succinate: ubiquinone reductase) was observed. Our results support the hypothesis of a wide-spread mitochondrial complex I deficiency in PD and MSA as compared to age-matched controls, who showed age-related deficiency. This deficit can be found in de novo PD patients as well as in treated patients. The observed respiratory enzyme chain deficiency could not be explained by the dose and duration of l-Dopa or dopaminergic agonist treatment, the severity of the disease, anxiety or depression since no significant correlation was found between these parameters and enzyme complexes activities.</abstract>
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