Figure 2

In the lung, the initial target for CNTs is probably type I epithelial cells whose necrotic death stimulates a proinflammatory response and recruitment of inflammatory cells. Interactions include oxidative burst due to activation of NADPH oxidase and possible interactions of nanoparticles with microbial pathogens. NADPH oxidase complex is activated in macrophages during inflammation and acts as the major source for generation of reactive oxygen species, such as superoxide O₂–d radicals that disproportionate to form hydrogen peroxide (H₂O₂). Transition metals, through their interactions with O₂–d and H₂O₂, act as catalysts for the formation of highly reactive hydroxyl (OH^·) radicals. Oxidatively modified lipids generated by cyclooxygenase (COX-2) and lipooxygenase (LOX) participate in amplification of the inflammatory response via recruitment of new inflammatory cells