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

Summary.

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.

Method. 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.

Interpretation. 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.