No evidence for altered muscle mitochondrial function in Parkinson's disease.
Recent reports indicate that reductions in mitochondrial respiratory chain function occur in substantia nigra, platelets, and muscle from patients with Parkinson's disease. To confirm and further characterise the presence of a generally distributed mitochondrial defect, mitochondrial metabolism was evaluated in muscle obtained from subjects with Parkinson's disease and from normal controls. Oxygen consumption rates in muscle mitochondria represented by complex I, complexes II-III, or complex IV did not differ between the two groups. Likewise, activities of rotenone sensitive NADH cytochrome c reductase, succinate cytochrome c reductase, or cytochrome oxidase in muscle mitochondria were not significantly different between Parkinsonian and control subjects. These findings fail to provide support for a generalised defect in mitochondrial function in Parkinson's disease but do not exclude an abnormality in respiratory function confined to the substantia nigra.
Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
J J
JJ
Anderson
D
D
Bravi
R
R
Ferrari
T L
TL
Davis
F
F
Baronti
T N
TN
Chase
F
F
Dagani
D000328:Adult; D000368:Aged; D000978:Antiparkinson Agents / Q000627:therapeutic use; D001927:Brain Diseases / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D008931:Mitochondria, Muscle / Q000201:enzymology / Q000378:metabolism; D009097:Multienzyme Complexes; D009245:NADH Dehydrogenase / Q000378:metabolism; D010101:Oxygen Consumption; D010300:Parkinson Disease / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D012129:Respiratory Function Tests; D013378:Substantia Nigra / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*
D000978:Antiparkinson Agents; D009097:Multienzyme Complexes; D007980:Levodopa; D009245:NADH Dehydrogenase