Engineered nanoceria modulate neutrophil oxidative response to low doses of UV-B radiation through the inhibition of reactive oxygen species production.

To avoid aging and ultraviolet mediated skin disease the cell repair machinery must work properly. Neutrophils, also known as polymorphonuclear leukocytes, are the first and most abundant cell types which infiltrate sites of irradiation and play an important role in restoring the microenvironment homeostasis. However, the infiltration of neutrophils in ultraviolet-B (UV-B) irradiated skin might also contribute to the pathophysiology of skin disease. The polymorphonuclear leukocytes activation induced by UV-B exposure may lead to prolonged, sustained NADPH oxidase activation followed by an increase in reactive oxygen species (ROS) production. Our previous work showed that cerium oxide nanoparticles can protect L929 fibroblasts from ultraviolet-B induced damage. Herein, we further our investigation of engineered cerium oxide nanoparticles (CNP) in conferring radiation protection specifically in modulation of neutrophils' oxidative response under low dose of UV-B radiation. Our data showed that even low doses of UV-B radiation activate neutrophils' oxidative response and that the antioxidant, ROS-sensitive redox activities of engineered CNPs are able to inhibit the effects of NADPH oxidase activation while conferring catalase and superoxide dismutase mimetic activity. Further, our investigations revealed similar levels of total ROS scavenging for both CNP formulations, despite substantial differences in cerium redox states and specific enzyme-mimetic reaction activity. We therefore determine that CNP activity in mitigating the effects of neutrophils' oxidative response, through the decrease of ROS and of cell damage such as chromatin condensation, suggests potential utility as a radio-protectant/therapeutic against UV-B damage.

Antioxidative photochemoprotector effects of cerium oxide nanoparticles on UVB irradiated fibroblast cells.

The Ultraviolet-B radiation (UVB) might induce cellular redox imbalance which plays an important role in the development of skin disorders. Thus, the search for photochemoprotective alternatives with antioxidant efficacy would be a safe aspect towards prevention of skin diseases. Cerium oxide nanoparticles (CNPs) have antioxidant properties, that are mostly related to CNPs catalase and superoxide dismutase (SOD)-like antioxidative mimetic activity. Considering that, we investigated whether CNPs induce photochemoprotection against UVB-induced cellular damages on L929 fibroblasts. Our results showed that CNPs prevented UVB mediated L929 cell oxidative damage by reestablishing the oxidative balance through ameliorating the reactive oxygen species (ROS) level and enhancing the antioxidant enzyme activities.