Scheme 1.

Graphical scheme of the experiments. The possible mechanism underlying UVB-induced corneal surface damages and the protection of fullerenol in corneal epithelial cell injury using in vitro and in vivo models. A, C) Schematic diagram of the corneal response to UVB radiation exposure. The corneal epithelial cells exposed to UVB produce reactive oxygen species (ROS) and peroxynitrite anion (ONOO⁻). The accumulation of free radicals is expected to cause oxidative stress and further single-strand breaks of DNA. Free radical-associated mitochondrial damage decreases mitochondrial membrane potential and disturbs the function of mitochondrial respiration chain. B, D) Schematic illustration of the protective mechanisms of fullerenol on the cell injury caused by UVB irradiation. Fullerenol easily penetrates the cell membrane and reacts with excessive radicals localized throughout the cytoplasm, quenches them by redox reactions. Upon oxidative DNA damage in nuclei, it traverses the nuclear envelope, promotes homologous recombination repair (HRR) and double-strand break repair.