Simultaneous Measurement of Mitochondrial Function and NO

There is increasing evidence to support the concept that defects in mitochondrial-energy metabolism may underlie the pathology of several disorders such as neurodegenerative diseases. The exact mechanisms involved in the pathogenesis of these disorders are not known, but it is thought that there may be excessive production of oxygen-derived free radicals (1 –2 ). Nitric oxide (NO) is a free radical that plays important roles in diverse physiological processes, such as vasodilatation, inhibition of platelet aggregation, and neurotransmission. However, it can also be toxic under certain conditions and it has been postulated that the mechanisms of cell damage by NO include an inhibition of a number of cellular processes, one of which is mitochondrial respiration (3 –5 ).