Potential Protective Effects of Cerium Oxide Nanoparticles on Ultraviolet-B Irradiated Fibroblast Cells

Increased environmental ultraviolet-B (UVB) exposure stimulates reactive oxygen species (ROS) overproduction, disrupts cellular redox balance, and contributes to skin disorders. Antioxidants inhibit autoxidation by neutralizing or suppressing free radicals. Certain nanomaterials, like cerium oxide nanoparticles (CNPs), function as antioxidants under specific conditions. Through their redox and catalytic properties, CNPs scavenge ROS, mitigate oxidative damage, and may help prevent skin injuries. While most research targets ionizing radiation, studies exploring CNPs under non-ionizing UVB remain limited. To address this, the study evaluates their photochemoprotective effects in UVB-exposed L929 fibroblasts. The 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), cupric ion reducing antioxidant capacity (CUPRAC), dichloro-dihydro-fluorescein diacetate (DCFH-DA), and annexin V/propidium iodide (annexin V/PI) assays were used to evaluate cell viability, oxidative stress, and apoptosis. Cell viability was assessed using the MTT assay at CNP concentrations of 10, 50, and 100 μM and UVB intensities of 150-900 mJ/cm², selected based on prior physiologically relevant in vitro studies. At 600 mJ/cm² UVB, cell viability decreased by 45% (MTT assay). Treatment with 50 μM CNP significantly increased total antioxidant capacity relative to untreated controls (CUPRAC assay, p = 0.0018). CNP and UVB effects on ROS production and apoptosis were evaluated separately and in combination using DCFH-DA and annexin V/PI assays. Results show that pretreatment with CNPs before UVB radiation impedes cell apoptosis and reduces ROS, suggesting that CNPs mitigate UVB-induced oxidative damage in L929 cells by restoring oxidative balance through their redox activity and ROS-scavenging properties. These findings indicate CNP-based interventions may offer therapeutic strategies against UVB-induced skin and related disorders.