Impaired oxidative decarboxylation of pyruvate in fibroblasts from patients with Parkinson's disease

Whether or not a reported deficiency in brain mitochondrial complex I activity in Parkinson's disease represents a defect encompassing other organs or tissues has been a source of some controversy. We have examined mitochondrial respiration in fibroblasts from patients with Parkinson's dis...

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Bibliographic Details
Published in:Journal of Neural Transmission - Parkinson's Disease and Dementia Section 1994-01, Vol.8 (3), p.223-228
Main Authors: MYTILINEOU, C, WERNER, P, MOLINARI, S, DI ROCCO, A, COHEN, G, YAHR, M. D
Format: Article
Language:English
Subjects:
Adult
Aged
Biological and medical sciences
Case-Control Studies
Cells, Cultured
Decarboxylation
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Evaluation Studies as Topic
Female
Fibroblasts - metabolism
Humans
Male
Medical sciences
Middle Aged
Mitochondria - metabolism
Neurology
Oxidation-Reduction
Oxygen Consumption - physiology
Parkinson Disease - diagnosis
Parkinson Disease - metabolism
Pyruvates - metabolism
Pyruvic Acid
Succinates - metabolism
Succinic Acid
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Summary:Whether or not a reported deficiency in brain mitochondrial complex I activity in Parkinson's disease represents a defect encompassing other organs or tissues has been a source of some controversy. We have examined mitochondrial respiration in fibroblasts from patients with Parkinson's disease by measuring the oxidative decarboxylation of [2-14C]pyruvate and [1,4-14C]succinate. We report that oxidation of pyruvate but not succinate was significantly reduced in fibroblasts from Parkinson patients when compared to healthy controls. These observations support the view that a widespread deficit in mitochondrial respiration exists in Parkinson's disease. Fibroblast cultures, moreover, are a source of affected proliferating cells, which can be used for in vitro studies of the nature of the respiratory defect and for testing of pharmacological interventions to correct the deficiency.
ISSN:0936-3076
1435-1463
DOI:10.1007/BF02260943