Oxidative stress and catalysis
Oxidative stress is often brought in context with nanotoxicology. It can be measured directly with dichlorofluorecein or indirectly by the upregulation of reactive oxygen species (ROS) eliminating enzymes like superoxide dismutase [34]. Another approach involves tests whether the nanoparticle dependent toxicity can be reduced by the application of an antioxidant. Widely used semiconductor materials such as lead sulfide nanoparticles may have the potential to generate oxidative stress in the lung. A recent study tested the toxicity of intratracheally applied 30 nm and 60 nm lead sulfide nanoparticles on rats. Oxidative damage was evaluated based on superoxide dismutase, total antioxidant capacity, and concentration of malondialdehyde. In addition to inflammatory responses, both 30 nm and 60 nm groups showed increased oxidative damage compared to control groups. The effect was significantly stronger for the 30 nm lead sulfide compared to the 60 nm nanoparticles [35]. Another nanomaterial which is associated with oxidative stress is nanosized titanium dioxide. Li et al. induced pulmonary injury in mice by daily intranasal instillation of suspended 294 nm TiO2 nanoparticles for 90 days,demonstrating that the rate of reactive oxygen species (ROS) generation increased with increasing TiO2 doses.Moreover lipid, protein and DNA peroxidation products were identified in elevated doses, which suggests that ROS dependent lung damage was significant in the nanoparticle treated animals [36]. Furthermore, in vitro tests on BEAS2B and A549 lung cell lines demonstrated that the commonly used nanoparticles ZnO and Fe2O3 are very different in terms of creating oxidative stress. The Fe 2O3 nanoparticles with an average diameter of 39 nm were distributed in the cytoplasm, whereas the 63 nm ZnO nanoparticles were trapped in organelles such as the endosome.In contrast to the Fe2O3 nanoparticles the ZnO nanoparticles caused reactive oxygen species production as well as cell cycle arrest, cell apoptosis, mitochondrial dysfunction and glucose metabolism perturbation [37] (Table 1).