The simultaneous regulation of multiple complex genes in the electron transport system in the six brain regions observed in the current work may indicate a beneficial effect of nicotine on the nervous system. However, the mechanisms underlying the modulation of nicotine-electron transport system interactions are unclear. One of the plausible possibilities is that nicotine, which can enter cells by permeating the membrane (Sallette et al. 2005), acts as an antioxidant (Obata et al. 2002; Soto-Otero et al. 2002) and eliminates the ROS generated by mitochondria. Such interaction may eventually lead to modulation of the activity of the electron transport system, thereby affecting ATP production (Halestrap 1987, 1989; Lim et al. 2002). It also is possible that nicotine interacts directly with one or more complexes of the electron transport system (Cormier et al. 2001, 2003; Xie et al. 2005). Because the 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
