Oxidative stress induced by engineered NP is due to acellular factors such as particle surface, size, composition, and presence of metals, while cellular responses such as mitochondrial respiration, NP-cell interaction, and immune cell activation are responsible for ROS-mediated damage. NP-induced oxidative stress responses are torch bearers for further pathophysiological effects including genotoxicity, inflammation, and fibrosis as demonstrated by activation of associated cell signaling pathways. Since oxidative stress is a key determinant of NP-induced injury, it is necessary to characterize the ROS response resulting from NP. Through physicochemical characterization and understanding of the multiple signaling cascades activated by NP-induced ROS, a systemic toxicity screen with oxidative stress as a predictive model for NP-induced injury can be developed.

The toxic potential of NPs is dependent on their size and shape, which determined their propensity to induce the generation of reactive oxygen species (ROS) [20, 21]. The excess generation ROS may induce an array of physiopathologic outcomes, including genotoxicity, apoptosis, necrosis, inflammation, fibrosis, metaplasia, hypertrophy, and carcinogenesis [18, 22, 23].