Ubiquinone Redox Status in Brain in Vitro

Abstract —The redox status of ubiquinone (Q) as an index of mitochondrial respiratory chain activity in chopped telencephalon from the rat was investigated. With 12mm‐glucose under aerobic conditions Q was 73% oxidized. Three mm‐amytal and 2 μm‐rotenone, inhibitors of mitochondrial NADH oxidation, resulted in Q being further oxidized by 14 and 16%, respectively. Thus, amytal and rotenone result in shifts in Q redox status of rat telencephalon slices in accord with the known site of action of these compounds in isolated mitochondria. However, under anaerobic conditions Q redox status shifted to 25% oxidized while incubation with 1 mm‐NaCN resulted in a shift to only 58% oxidized. This discrepancy may result from concomitant inhibition in the supply of reducing equivalents to Q from substrate by NaCN or it may reflect a differential sensitivity of neuronal and glial mitochondria to NaCN. Evaluation of Q oxidation‐reduction can be used to measure the effects of drugs and physiological perturbations on the redox status of the mitochondrial compartment of intact brain preparations.