Goetz 2000 J Neural Transm (Vienna)
|Götz ME, Gerstner A, Harth R, Dirr A, Janetzky B, Kuhn W, Riederer P, Gerlach M (2000) Altered redox state of platelet coenzyme Q10 in Parkinson's disease. J Neural Transm (Vienna) 107:41-8.|
Abstract: The reduced form of coenzyme Q10 (CoQQ10) acts as a lipophilic antioxidant and participates in electron and proton transport of the respiratory chain in the inner mitochondrial membrane. An alteration in CoQQ10 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 CoQQ10 redox state.
We have determined concentrations of the reduced and oxidized forms of CoQQ10 and the activity of monoamine oxidase B in platelets isolated from parkinsonian patients and age- and gender-matched controls.
Platelet CoQQ10 redox ratios (reduced CoQQ10 to oxidized CoQQ10) and the ratio of the reduced form, compared with total platelet CoQQ10, were significantly decreased in de novo parkinsonian patients. Platelet CoQQ10 redox ratios were further decreased by L-DOPA treatment (not significant), whilst selegiline treatment partially restored CoQQ10 redox ratios. Monoamine oxidase activities in non-selegiline treated patients were similar to controls.
Our results either suggest an impairment of electron transport or a higher need for reduced forms of CoQQ10 in the platelets of even de novo parkinsonian patients. However, the CoQQ10 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.
• Bioblast editor: Plangger M
Regulation: Q-junction effect