4.5 Article

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

Journal

JOURNAL OF BIOMEDICAL MATERIALS RESEARCH PART A
Volume 109, Issue 12, Pages 2570-2579

Publisher

WILEY
DOI: 10.1002/jbm.a.37251

Keywords

antioxidant; cerium oxide nanoparticles; homeostasis; neutrophils; UV-B

Funding

  1. NSF MRI XPS: ECCS [1726636]
  2. Programa de Apoio a Nucleos de Excelencia (PRONEX)/Fundacao Araucaria andComplexo de Centrais de Apoio a Pesquisa (COMCAP)-Universidade Estadual de Maringa
  3. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
  4. Conselho Nacional de Desenvolvimento cientifico e Tecnologico (CNPq)

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Neutrophils play a crucial role in restoring skin microenvironment homeostasis, but their activation under UV-B exposure can lead to increased production of reactive oxygen species. Engineered cerium oxide nanoparticles show potential in mitigating the effects of neutrophils' oxidative response and protecting against UV-B induced skin damage.
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.

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