Altered redox state of platelet coenzyme Q10 in Parkinson's disease

Background. The reduced form of coenzyme Q(10) (CoQ(10)) acts as a lipophilic antioxidant and participates in electron and proton transport of the respiratory chain in the inner mitochondrial membrane. An alteration in CoQ(10) 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 CoQ(10) redox state. Method. We have determined concentrations of the reduced and oxidized forms of CoQ(10) and the activity of monoamine oxidase B in platelets isolated from parkinsonian patients and age- and gender-matched controls. Results. Platelet CoQ(10) redox ratios (reduced CoQ(10) to oxidized CoQ(10)) and the ratio of the reduced form, compared with total platelet CoQ(10), were significantly decreased in de novo parkinsonian patients. Platelet CoQ(10) redox ratios were further decreased by L-DOPA treatment (not significant), whilst selegiline treatment partially restored CoQ(10) redox ratios. Monoamine oxidase activities in non-selegiline treated patients were similar to controls. Interpretation. Our results either suggest an impairment of electron transport or a higher need for reduced forms of CoQ(10) in the platelets of even de novo parkinsonian patients. However, the CoQ(10) 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.