Quantitative study of mitochondrial complex I in platelets of parkinsonian patients

Fabio Blandini, Giuseppe Nappi, J. Timothy Greenamyre

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Activity of mitochondrial enzyme complex I (NADH-ubiquinone oxidoreductase) is reduced in the substantia nigra of patients with Parkinson's disease (PD). A less pronounced decrease in the activity of this enzyme has also been reported in platelets of PD patients. To obtain quantitative information on platelet complex I in PD, we studied platelet complex I in 16 PD patients and 16 age-matched controls by using a newly developed technique based on the binding of [3H]dihydrorotenone ([3H]DHR), an analog of the pesticide rotenone, to complex I. We also investigated the inhibitory effect of MPP+ (1-methyl-4-phenyl-pyridinium) on [3H]DHR specific binding to platelet complex I. PD patients and controls showed similar levels of [3H]DHR specific binding; preincubation of platelets with MPP+ caused the same degree of inhibition of [3H]DHR specific binding in the two groups. In PD patients, we observed a direct correlation between MPP+-induced inhibition of [3H]DHR specific binding and the daily intake of levodopa, which may be related to drug-induced changes in the transport of MPP+ into the platelet or in its binding to complex I. These findings demonstrate that the reported reduction in complex I activity in platelets of PD patients can not be accounted for by an abnormality at the level of the rotenone binding site (putatively the ND-1 gene product), although they do not exclude differences in complex I activity between PD patients and controls.

Original languageEnglish
Pages (from-to)11-15
Number of pages5
JournalMovement Disorders
Issue number1
Publication statusPublished - 1998


  • 1-Methyl-4-phenyl-pyridinium (MPP)
  • [H]dihydrorotenone
  • Complex I
  • Energy metabolism
  • Mitochondria
  • Parkinson's disease
  • Platelet

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)


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