Mitochondria are central for cellular energy metabolism, respiration and production of reactive oxygen species (ROS) making them easy targets for xenobiotics. Plastic nanoparticles (NPs) represent an emerging threat to exposed organisms and their effects were examined in mitochondria. The goal of this study was to examine changes in the fractal dimension of mitochondria caused by selected environmental contaminants such polystyrene nanoparticles (NPs). Mitochondria from Elliptio complanata mussels were isolated and exposed in vitro to selected environmental chemicals: nicotine (Nic), isoniazid (Iso), ibuprofen (Ibu), erbium (Er), lutetium (Lu), zinc oxide and polystyrene NPs for one h at 25 °C. The activity in NADH oxidase, the oscillatory behavior in NADH levels and the fractal dimension were determined during that time. The following compounds were able to accelerate the reaction rate of NADH oxidase, which are the main source of ROS in cells: Nic and Iso. Zinc oxide NP decreased NADH oxidase. Nic and Iso also reduced the fractal dimension (fD) of NADH changes, which was consistent with the nicotinic acetylcholine receptor pathway in blocking mitochondrial permeability transition pores. NADH levels oscillated during the exposure period and revealed a frequency dependent decay in amplitudes consistent with a fractal environment. Nic, Iso and polystyrene NPs were able to decrease the fD and the appearance of low amplitude frequencies. The fractal properties of NADH changes in time revealed that reduced dimensions leading to increased NADH oxidase activity by polystyrene NPs. This could form the basis of polystyrene NP-induced oxidative stress in organisms.