Figure 2.

Effect of α-synuclein on NADH redox state in cells with mitochondrial mutations and control neurons. Estimation of the percentage change in mitochondrial NADH pool in control cells—control (b), complex I deficient (c) and cells with a deficiency of complex IV (d). (a) Redox state was estimated as: 0 is response to FCCP (maximal rate of respiration and lowest level of mitochondrial NADH) and 100% is response to cyanide (inhibition of respiration with no consumption of NADH in mitochondria); complex I- and complex IV-deficient neurons have higher NADH redox state compared with control neurons (**P<0.001). Treatment with 100 nM α-synuclein increased both the level of NADH autofluorescence within WT neurons and the redox state (e). (f) How the effect of α-synuclein treatment on WT neurons compares to neurons with mitochondrial deficiencies. An increase in NADH autofluorescence following treatment is recorded in complex IV-deficient neurons suggesting CI inhibition, but not in complex I-deficient neurons.**P<0.001