Bravi D, Anderson J J, Dagani F, Davis T L, Ferrari R, Gillespie M, Chase T N
Experimental Therapeutics Branch, NINDS, NIH, Bethesda, Maryland 20892.
Mov Disord. 1992;7(3):228-31. doi: 10.1002/mds.870070307.
Oxygen consumption and enzyme activity were evaluated in platelet mitochondria from 17 patients with Parkinson's disease. In comparison with age-matched controls, no consistent abnormality could be discerned in complex I, complex II-III, or complex IV oxygen consumption, or in the enzyme activity of these respiratory chain complexes. Neither chronic therapy with levodopa/carbidopa alone nor in combination with deprenyl significantly affected any measure of mitochondrial respiratory function. There was no discernible relationship between patient age or disease severity and any parameter of mitochondrial respiration. Moreover, blood lactate levels following glucose loading were not different in patients and controls. These results fail to support the occurrence of a generalized defect in any mitochondrial respiratory function in Parkinson's disease.
