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Cited by 44Parkinson's Disease Mechanisms and TreatmentsMitochondrial Function and PathologyCoenzyme Q10 studies and effects

Quantitative study of mitochondrial complex I in platelets of parkinsonian patients

Blandini, Fabio, Nappi, Giuseppe, Timothy Greenamyre, J.·1998·Movement Disorders
DOI 10.1002/mds.870130106
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Abstract

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 [3 H]dihydrorotenone ([3 H]DHR), an analog of the pesticide rotenone, to complex I. We also investigated the inhibitory effect of MPP+ (1‐methyl‐4‐phenyl‐pyridinium) on [3 H]DHR specific binding to platelet complex I. PD patients and controls showed similar levels of [3 H]DHR specific binding; preincubation of platelets with MPP+ caused the same degree of inhibition of [3 H]DHR specific binding in the two groups. In PD patients, we observed a direct correlation between MPP+‐induced inhibition of [3 H]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.

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  • Impairment of mitochondrial complex-I activity has been observed in the substantia nigra, platelets, and skeletal muscle of PD patients, in some but not all studies.

    “An impairment of mitochondrial complex-I activity has been observed in the substantia nigra (SN), platelets, and skeletal muscle of PD patients 1, 9-13, in some but not in all studies14, 15.”

    From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [15]

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Authors
Blandini, F., Nappi, G., & Timothy Greenamyre, J.
Affiliations
University of Pavia (IT)
Corresponding author
Blandini, Fabio
ORCID
Venue
Movement Disorders
Publisher
Wiley
Published
1998-01
Volume
13
Issue
1
Pages
11-15
ISSN
  • 0885-3185 (ISSN-L)
  • 1531-8257
DOI
10.1002/mds.870130106
OpenAlex
W2161036732
Cited by
44
References
30
Citations by year
2025: 1 · 2024: 1 · 2023: 2 · 2021: 3 · 2019: 2 · 2018: 2 · 2017: 1 · 2015: 3 · 2014: 3 · 2013: 2 · 2012: 2
FWCI
1.03
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 2499 d)
Locations
  • Movement Disorders (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Neurological Disorders and Stroke (NS33779, R01NS033779)
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
Keywords
Parkinson's disease, mitochondrial complex I, platelets, complex I, levodopa, substantia nigra
MeSH terms
Aged, Aged, 80 and over, Blood Platelets, Dose-Response Relationship, Drug, Female, Humans, Insecticides, Male, Middle Aged, Mitochondria, NADH, NADPH Oxidoreductases, Neurotoxins, Parkinson Disease, Radioligand Assay, Rotenone, Dopamine Agents, 1-Methyl-4-phenylpyridinium, Case-Control Studies, Electron Transport Complex I

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