Bruin et al. 2008c). When colon adenocarcinoma-derived HCT-116 cells were treated with nicotine at a concentration similar to that in a smoker, an alteration in mitochondrial membrane potential and an increase in oxidative stress and apoptosis were noted (Crowley-Weber et al. 2003). In another study, nicotine proved to be antiapoptotic, modulating mitochondrial signaling pathways and inhibiting chemotherapy-induced apoptosis in lung cancer (Zhang et al. 2008). Nicotine treatment also can regulate the activity of mitochondria in the brain. Both acute and chronic nicotine treatment lead to increases in the expression of malate dehydrogenase and succinate dehydrogenase of the mitochondrial Krebs cycle in the rat frontoparietal cortex, but not in other regions of the brain (Turegano et al. 2001). There also is evidence that chronic nicotine treatment induces oxidative stress greatly and increases the amount of mitochondrial glutathione S-transferase, the major cellular antioxidant component, in rat brain (Bhagwat et al. 1998).
