electron transport complexes are physically interdependent, regulation of any of their genes may result in modulation of the expression of genes of other complexes. For example, mutation of complex I genes results not only in complex I deficiency, but also in reduction of complex III activity (Budde et al. 2000). Further, mutations of the complex III gene Mt-cyb cause combined instability and reduced activity of complexes I and complex III (Blakely et al. 2005). On the other hand, nicotine may regulate other biochemical pathways in mitochondria through intracellular signaling pathways. In the nervous system, nicotine exerts its effect mainly through its interaction with nAChRs. Activation of nAChRs causes membrane depolarization and directly and indirectly increases the intracellular calcium concentration (McKay et al. 2007). The variation of cytosolic calcium concentration may influence the calcium homeostasis of mitochondria (Rimessi et al. 2008). The Ca2+ homeostasis is fundamental to the function of mitochondria and related to the generation of ATP, ROS, and a series of signaling pathways critical to cell life (Rego and Oliveira 2003; Rimessi et al. 2008; Szabadkai and Duchen 2008). Recent work also has demonstrated that these pathways, including the protein kinase A (PKA) and C (PKC) signaling cascades, are
