Among the organelles affected by nicotine treatment, the mitochondrion is of particular interest because it is responsible for the generation of most usable energy and is the principal source of reactive oxygen species (ROS) in a cell. In addition, mitochondria play an important role in many physiological processes such as apoptosis and proliferation. However, the effect of nicotine on mitochondria appears to be complicated. For example, rats receiving nicotine showed alterations in mitochondrial ultrastructure such as irregular cristae and an electron-dense matrix in testis (Aydos et al. 2001), and dilated mitochondria were observed in nicotine-treated rat gingival fibroblasts (Lahmouzi et al. 2000). Fetal and neonatal exposure to nicotine also leads to detrimental changes in the mitochondria of postnatal pancreatic tissues, such as volume swelling, reduced respiratory chain activity, and increased oxidative stress (Bruin et al. 2008a; Bruin et al. 2008b; 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
