title: Altered redox state of platelet coenzyme Q10 in Parkinson's disease.
abstract: BACKGROUND
  The reduced form of coenzyme Q10 (CoQ10) acts as a lipophilic antioxidant and participates in electron and proton transport of the respiratory chain in the inner mitochondrial membrane. An alteration in CoQ10 redox state may thus reflect a change in membrane electron transport and the effectiveness of defense against toxic reactive oxygen species such as hydrogen peroxide and superoxide. In Parkinson's disease alterations in the activities of complex I have been reported in substantia nigra and platelets. Deficiency of mitochondrial enzyme activities could affect electron transport which might be reflected by the platelet CoQ10 redox state.
  
  
  METHODS
  We have determined concentrations of the reduced and oxidized forms of CoQ10 and the activity of monoamine oxidase B in platelets isolated from parkinsonian patients and age- and gender-matched controls.
  
  
  RESULTS
  Platelet CoQ10 redox ratios (reduced CoQ10 to oxidized CoQ10) and the ratio of the reduced form, compared with total platelet CoQ10, were significantly decreased in de novo parkinsonian patients. Platelet CoQ10 redox ratios were further decreased by L-DOPA treatment (not significant), whilst selegiline treatment partially restored CoQ10 redox ratios. Monoamine oxidase activities in non-selegiline treated patients were similar to controls.
  
  
  CONCLUSIONS
  Our results either suggest an impairment of electron transport or a higher need for reduced forms of CoQ10 in the platelets of even de novo parkinsonian patients. However, the CoQ10 redox ratio was not correlated to disease severity, as determined by the Hoehn and Yahr PD disability classification, suggesting that this parameter may not be useful as a peripheral trait marker for the severity of PD but as an early state marker of PD.
authors.affiliation: Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Federal Republic of Germany.
authors.forename: M E
authors.initials: ME
authors.lastname: Götz
authors.forename: A
authors.initials: A
authors.lastname: Gerstner
authors.forename: R
authors.initials: R
authors.lastname: Harth
authors.forename: A
authors.initials: A
authors.lastname: Dirr
authors.forename: B
authors.initials: B
authors.lastname: Janetzky
authors.forename: W
authors.initials: W
authors.lastname: Kuhn
authors.forename: P
authors.initials: P
authors.lastname: Riederer
authors.forename: M
authors.initials: M
authors.lastname: Gerlach
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000975:Antioxidants / Q000378:metabolism*; D000978:Antiparkinson Agents / Q000008:administration & dosage; D015415:Biomarkers; D001792:Blood Platelets / Q000201:enzymology*; D003067:Coenzymes; D005260:Female; D006801:Humans; D007980:Levodopa / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D008995:Monoamine Oxidase / Q000378:metabolism; D010084:Oxidation-Reduction; D010300:Parkinson Disease / Q000188:drug therapy / Q000201:enzymology*; D012642:Selegiline / Q000008:administration & dosage; D014451:Ubiquinone / Q000031:analogs & derivatives* / Q000378:metabolism
chemical_list: D000975:Antioxidants; D000978:Antiparkinson Agents; D015415:Biomarkers; D003067:Coenzymes; D014451:Ubiquinone; D012642:Selegiline; D007980:Levodopa; D008995:Monoamine Oxidase; C024989:coenzyme Q10