Defects of any gene in the electron transport system can disturb this system and interrupt the activity of mitochondria. For example, mutations of Mt-cyb have been associated with deficiency in complex III function and impaired mitochondrial activity (Dumoulin et al. 1996; Legros et al. 2001). Moreover, dysfunction of the mitochondrial electron transport system is implicated in several pathogenic conditions, including neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) (Lin and Beal 2006). A significant and selective reduction of complex I activity was found in the substantia nigra of patients with PD. It has been reported also that a null mutation of Mt-cyb results in deficiency of complex III and an increase in free radical production in brain tissues of patients with PD (Rana et al. 2000). A deficiency of cytochrome c oxidase (complex IV) also can cause defects in energy metabolism in the brain and peripheral tissue, which may contribute to the neurodegenerative condition in AD patients (Grazina et al. 2006; Qiu et al. 2001). In these diseases, the damage to mitochondria or their components may increase production of ROS, which leads to the death of the neuron.
